Note: This is not an exhaustive list.
When time allows more information will be added.

Ammonium fluoride - Wood Preservative - CAS No. 12125-01-8

Ingestion: May cause salivation, nausea, vomiting, diarrhea, and abdominal pain, followed by weakness, tremors, shallow respiration, cardopedal spasm, convulsions, and coma. May cause brain and kidney damage. Death may be caused by respiratory paralysis. Affects heart and circulatory system.
Chronic Exposure: Chronic exposure may cause mottling of teeth and bone damage (osteosclerosis) and fluorosis. Symptoms of fluorisis include brittle bones, weight loss, anemia, calcified ligaments, general ill health and joint stiffness.
Ref: 1999 Material Safety Data Sheet prepared by Mallinckrodt Baker, Inc.
http://www.fluoridealert.org/pesticides/Ammonium.F.MSDS.htm

-- INHALATION - May cause severe throat irritation, cough, dyspnea, cyanosis, lung injury and noncardiogenic pulmonary edema.
-- RESPIRATORY. ACUTE EXPOSURE. Dyspnea, bronchospasm (with abnormal PFTs and hypoxia), chemical pneumonitis, pulmonary edema (can be hemorrhagic), tracheobronchitis, upper airway obstruction, chemical burns (larynx, trachea, bronchi) and ARDS may occur following inhalation.
Ref: TOXNET profile from Hazardous Substances Data Bank for Ammonium fluoride.
http://www.fluoridealert.org/pesticides/Ammonium.fluoride.TOXNET.htm

Benzotrifluoride - Insecticide - CAS No. 98-08-8

TARGET ORGANS: Central Nervous System, Eyes, Skin, Respiratory Tract.
Ref: BENZOTRIFLUORIDE Material Safety Data Sheet. OxyChem. Issue Date: 07-08-98
http://www.oxychem.com/products/msds/m7644.pdf

SYMPTOMS: This comound is extremely destructive to the mucous membranes, upper respiratory tract, skin and eyes. Inhalation may be fatal as a result of spasm, inflammation and edema of the larynx and bronchi; chemical pneumonitis and pulmonary edema. Other symptoms include a burning sensation, coughing, wheezing, laryngitis, shortness of breath; headache, nausea and vomiting.
Ref: 1987 Fact Sheet by National Toxicology Program for Benzotrifluoride.
http://www.fluoridealert.org/pesticides/Benzotrifluoride.1987.NTP.htm

Beta-cyfluthrin - Insecticide - CAS No. 68359-37-5

-- Beta-cyfluthrin (98% a.i.). 5-Day range-finding NOAEL = 0.00025 mg/L (0.07 mg/kg/day) inhalation study--rat LOAEL = 0.0038 mg/L (1.03 mg/kg/day) based on unpreened hair coat, piloerection, hepatoid foci in lungs.
Ref: Federal Register. September 27, 2002. Cyfluthrin; Pesticide Tolerance. Final Rule. http://www.fluoridealert.org/pesticides/Cyfluthrin.FR.Sept.27.2002.htm

Bifenthrin - Acaricide, Insecticide - CAS Numbers: 82657-04-3 (Cis); 83322-02-5 (Trans)

A chronic/carcinogenicity study in mice fed at doses of 0, 50, 200, 500, or 600 ppm (0, 2.5, 10, 25, or 30 mg/kg/day) in the diet for 87 weeks (males) or 92 weeks (females). Chronic LOEL is 10 mg/kg/day based on the incidence of tremors in both sexes. Chronic NOEL is 2.5 mg/kg/day. Carcinogenic potential was evidenced by a statistically significant increased trend for hemangiopericytomas in the urinary bladders of males, a significant dose-related trend for combined hepatocellular adenomas and carcinomas in males, and a significantly higher incidence of combined lung adenomas and carcinomas in females.
Ref: Federal Register: November 26, 1997. Bifenthrin; Pesticide Tolerances. Final Rule.
http://www.fluoridealert.org/pesticides/bifenthrin.fr.nov.1997.htm

Carcinogenic Effects: There was no evidence of cancer in a 2-year study of rats who ate as much as 10 mg/kg/day of bifenthrin. However, an 87 week feeding study of mice with doses of 7, 29, 71, and 86 mg/kg showed a significantly higher, dose related trend of increased tumor incidence in the male urinary bladder (63, 67). The incidence was significantly increased at 86 mg/kg/day. Also, females had higher incidences of lung cancer than the controls at doses of 7 mg/kg and higher (67). The EPA has classified bifenthrin as a class C carcinogen, a possible human carcinogen (11, 63).
Ref: EXTOXNET Pesticide Information Profile. 1995.
http://ace.ace.orst.edu/info/extoxnet/pips/bifenthr.htm

Boron Trifluoride - Fumigant - CAS No. 7637-07-2

-- Target Organs: Lungs, blood, bones and teeth.
-- Signs and Symptoms of Exposure: Acute exposure: coughing, shortness of breath, headache, vertigo, chills and nausea. Subchronic: dental fluorosis, increased bone, serum and urinary fluoride levels, hypocalcemia.
-- Chronic and Subchronic Data: Two of forty rats exposed to 6 ppm for 6 hours/day, 5 days/week for 13 weeks exhibited renal toxicity and signs of respiratory irritation. Six month exposures of rats, rabbits and guinea pigs produced dental fluorosis and pneumonitis at similar levels. This material is listed in the Registry of Toxic Effects of Chemical Substances (RTECS), but no information on its carcinogenicity is available.
Ref: Material Safety Data Sheet for Boron Trifluoride (BF3). May 2001.
http://www.fluoridealert.org/pesticides/boron.trifluoride.msds.htm

-- Clinical Effects: SUMMARY OF EXPOSURE 0.2.1.1 ACUTE EXPOSURE to Boron trifluoride is a severe irritant to the lungs and eyes and corrosive on skin contact. Effects are similar to that of hydrogen fluoride but less severe.
-- CHRONIC EXPOSURE o Lowered pulmonary function, dried mucous membranes and nosebleeds, severe irritation of the eyes and eyelids, as well as inflammation and congestion of the lungs may occur with chronic exposure to this compound (HSDB, 1992).
-- Exposure of 6 animal species to 100 ppm, 4-7 hr/day, 5 days/wk in a 30 day experiment killed all animals, most within the test period. Guinea pigs were most susceptible ... dogs least ... The primary site of damage was the lung ... Kidney damage ... also occurs. [Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) PublicationNo. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981. 1]
-- Boron trifluoride is primarily a respiratory irritant which predisposed the exposed /guinea pigs/ to respiratory infection. Exposure at 100 ppm (277 mg/cu m) was fatal to all animals. Physiological responses prior to death included respiratory irritation and infection, kidney damage, retarded growth, and severe progressive fluorosis in rat teeth. Exposure at 15 ppm (41.5 mg/cu m) did not produce fluorosis, but did predispose guinea pigs to a rate of respiratory infection greater than that found in controls. [NIOSH; Criteria Document: Boron trifluoride p.27 (1976) DHEW Pub. NIOSH 77-122]
-- Ten male guinea pigs and 14 female rats were exposed to boron trifluoride at a nominal concentration of 12.8 ppm (35 mg/cu m), 7 hours/day, 5 days/week, for up to 3 months. Examinations showed the guinea pigs had difficulty in breathing and appeared asthmatic. Exposed guinea pigs had increased lung weights averaging 0.80 g/100 g of body weight, compared to lung weights of 0.64 g/100 of body weight for the control animals. Gross examination revealed pneumonitis, suggesting chemical damage, in the hilar region of the lungs. Examined microscopically, the lung showed areas of collapse and emphysema adjacent to the areas of more severe pneumonitis. The exposed rats were considered to have normal appearance and organ weights, but gross and microscopic tissue examination showed pulmonary changes indicating chemical irritation. The hilar regions of the lung were the most affected and the injuries were manifested as pneumonitis. [NIOSH; Criteria Document: Boron trifluoride p.29-30 (1976) DHEW Pub. NIOSH 77-122]
Ref: TOXNET profile from Hazardous Substances Data Bank for Boron Trifluoride.
http://www.fluoridealert.org/pesticides/boron.trifluoride.toxnet.htm

Bromethalin - Rodenticide - CAS No. 63333-35-7

Abstract: Bromethalin is a new rodenticide for the control of commensal rodents. Doses in excess of the LD50 (2 mg/kg in rats) will cause death within 8-12 hr and it is preceded by one to three episodes of clonic convulsions with death usually due to respiratory arrest.
Ref: Fundam Appl Toxicol 1988 Nov;11(4):664-72. The toxicity and mechanism of action of bromethalin: a new single-feeding rodenticide by van Lier RB and Cherry LD.

Carbon Tetrafluoride - Former US EPA List 3 Inert - CAS No. 75-73-0

-- TARGET ORGANS: Respiratory system, cardio-vascular system, central nervous system.
-- ACUTE: The most significant hazard associated with Tetrafluoromethane [carbon tetrafluoride] is inhalation of high concentrations of Tetrafluoromethane. Such overexposure can cause oxygen deficiency. Symptoms of such exposures include respiratory difficulty, ringing in ears, headaches, dizziness, indigestion, nausea, and possible death...
-- INHALATION: Exposures to high concentrations of this gas may cause sensitization of the heart to adrenaline and nor-adrenaline. Effects of such overexposure can include light-headedness, giddiness, shortness of breath and in extreme cases, irregular heartbeats, cardiac arrest, and death. High concentrations of this gas can cause an oxygen-deficient environment. Individuals breathing such an atmosphere may experience symptoms which include headaches, ringing in ears, dizziness, drowsiness, unconsciousness, nausea, vomiting, and depression of all the senses. The skin of a victim of overexposure may have a blue color. Under some circumstances of overexposure, death may occur. The effects associated with various levels of oxygen are as follows:
CONCENTRATION SYMPTOMS OF EXPOSURE
12-16% Oxygen: Breathing and pulse rate increased, muscular coordination slightly disturbed.
10-14% Oxygen: Emotional upset, abnormal fatigue, disturbed respiration.
6-10% Oxygen: Nausea and vomiting, collapse or loss of consciousness.
Below 6%: Convulsive movements, possible respiratory collapse, and death.
Ref: Material Safety Data Sheet: TETRAFLUOROMETHANE - CF4 MSDS (Document # 001051). Airgas.
http://www.airgas.com/documents/pdf/1051.pdf

1-chloro-1,1-difluoroethane - Solvent, EPA Inert List 2 - CAS No. 75-68-3

Lester and Greenberg (1950) conducted whole-body exposures in 10 rats (sex and strain unspecified) to 100,000 ppm (413,100 mg/cu.m) for 16 hours/day. All animals died within nine exposures: 6 in 7 days, 2 in 8 days, and 2 in 9 days. All animals were examined grossly, and sections of lung and liver were examined for histopathology. Lungs of all animals showed signs of severe irritation, having extensive consolidation and advanced lobar pneumonia. In a subsequent experiment, five rats were exposed to 10,000 ppm (41,310 mg/cu.m), 16 hours daily for a period of 2 months, with no apparent effects. The lungs of 2/5 of these animals revealed evidence of inflammation, but sufficient information is not given to conclude that this effect was treatment related. These studies have a number of significant experimental (apparently no control animals were used) and reporting deficiencies that preclude their use in quantitative risk assessment.
Ref: US EPA IRIS for 1-Chloro-1,1-difluoroethane CASRN 75-68-3.
http://www.fluoridealert.org/pesticides/1-chloro-1.1-difluoroe.iris.htm

-- RESPIRATORY. ACUTE EXPOSURE. Pulmonary irritation, bronchial constriction, cough, dyspnea, and chest tightness may develop after inhalation. Chronic pulmonary hyperreactivity may occur. Adult respiratory distress syndrome has been reported following acute inhalational exposures. Pulmonary edema is an autopsy finding in fatal cases.
-- Populations at Special Risk: THERE ARE ISOLATED REPORTS OF POISONING FROM EXPOSURE TO FLUOROCARBON PROPELLANTS & SOME STUDIES SHOWING A HIGHER INCIDENCE OF CORONARY HEART DISEASE AMONG HOSPITAL PERSONNEL & REFRIGERANT MECHANICS EXPOSED TO FLUOROCARBONS. ADDITIONAL INVESTIGATION IS REQUIRED TO ESTABLISH CAUSAL RELATIONSHIP BETWEEN FLUOROCARBONS & CARDIOVASCULAR & BRONCHOPULMONARY DISEASES AMONG EXPOSED WORKERS. THE HIGH INCIDENCE OF CANCER AMONG HOSPITAL PERSONNEL REPEATEDLY EXPOSED TO FLUORINE-CONTAINING GENERAL ANESTHETICS RAISES A FUNDAMENTAL NEED TO EXAMINE OTHER FLUOROCARBON-EXPOSED WORKERS FOR SIMILAR EFFECTS. /FLUOROCARBONS/ [Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994. 1209]
Ref: TOXNET profile from Hazardous Substances Data Bank for 1-Chloro-1,1-Difluoroethane.
http://www.fluoridealert.org/pesticides/1-chloro-1,1,-difluo.toxnet.htm

Chlorodifluoromethane - Insecticide, Fungicide, Propellant - CAS No. 75-45-6

Animal Data - INHALATION: 4 hour, LC50, rat: 220,000 ppm. The compound is a skin irritant and a slight eye irritant, but is not a skin sensitizer in animals. Effects from single high exposures include central nervous system depression, anesthesia, rapid breathing, lung congestion and microscopic liver changes...
Ref: Material Safety Data Sheet for Freon 22. DuPont. 1996.

Cyfluthrin - Insecticide - CAS No. 68359-37-5

Prenatal and postnatal sensitivity. There are no data gaps for reproductive and developmental toxicity studies. Evidence of increased sensitivity of young rats following pre- and/or post-natal exposure to cyfluthrin was observed in the three-generation reproduction study in rats. There was suggestive sensitivity of rats to in utero exposure based on bradypnea seen in dams in the developmental inhalation studies. In addition, the reproductive NOAEL of 2.5 mg/kg/day and the LOAEL of 7.5 mg/kg/day established in the three-generation reproduction study in rats are identical to the systemic NOAEL/LOAEL of 2.5/7.5 mg/ kg/day established in the chronic toxicity/carcinogenicity study in rats. This NOAEL (2.5 mg/kg/day) and a UF of 100 was used in deriving the RfD (0.025 mg/kg/day) and the RfD does not provide protection for infants and children.
Ref: Federal Register. May 17, 2001, Pesticide Tolerances for Emergency Exemptions. Final Rule.
http://www.fluoridealert.org/pesticides/Cyfluthrin.FR.May17.2001.htm

Dichlorodifluoromethane - Insecticide, Fungicide, Propellant, US EPA List 2 Inert - CAS No. 75-71-8

-- 11 subjects (7 being maintenance technicians of large cooling and refrigerating systems) were exposed for 130 min to CFC-12 (weighted exposure 0.46, 49.9, and 87.7 g/cu m. ... This led to acute reduction of ventilatory lung capacity only at the two highest CFC-12 concentrations, under which conditions a significant decrease in the heart frequency was also observed. [WHO; Environmental Health Criteria 113: Fully Halogenated Chlorofluorocarbons p.90 (1990)]
-- Ten subjects /were exposed/ to CFC-11, CFC-12, CFC-114, two mixtures of CFC-11 and CFC-12, and a mixture of CFC-12 and CFC-114 (breathing concentrations between 16 and 150 g/cu m) for 15, 45, or 60 seconds, and found significant acute reduction of ventilatory lung capacity (FEV50, FEF25) on exposure to each chlorofluorocarbon, as well as bradycardia and increased variability in heart rate in seven subjects, negative T-waves in two subjects (one was exposed to CFC-11 and CFC-12), and atrioventricular block in 1 subject (CFC-114). Mixtures exerted stronger respiratory effects than individual chlorofluorocarbon at the same level of exposure. [WHO; Environmental Health Criteria 113: Fully Halogenated Chlorofluorocarbons p.90 (1990)]
-- Dichlorodifluoromethane ... /was/ tested by inhalation on Sprague-Dawley rats and Swiss mice. The animals were exposed for 4 hr a day, 5 days a week; rats were exposed for 104 weeks, and mice were exposed for 78 weeks. Animals were observed until spontaneous death. Exposure of rats to dichlorodifluoromethane resulted in no noticeable differences in the incidence of total benign and malignant tumors, and of the most frequently expected or rate of tumors. Exposure of mice to dichlorodifluoromethane resulted in a higher number of total tumors in males and females which was dose related in males, pulmonary adenomas in males and females at 5000 ppm, and leukemias in males at 5000 and 1000 ppm and in females at 1000 ppm. [Maltoni C et al; Annals of the New York Academy of Sciences 534: 261-82 (1988)]
-- Short-term inhalation studies have been reported for CFC-11, CFC-12, CFC-112, CFC-113, CFC-114, and CFC-115. The results showed low toxicity, and the effects observed were related mainly to the CNS, respiratory tract, and the liver. Oral toxicity studies have confirmed the low toxicity. [WHO; Environmental Health Criteria 113: Fully Halogenated Chlorofluorocarbons p.18 (1990)]
Ref: TOXNET profile from Hazardous Substances Data Bank for Dichlorodifluoromethane.
http://www.fluoridealert.org/pesticides/dichlorodifluorometh.toxnet.htm

Dichlorofluoromethane (CFC-21) - Propellant, EPA List 2 Inert - CAS No. 75-43-4

--Skin, Eye and Respiratory Irritations: Refrigerant 21 vapor is respiratory irritant ... [Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) PublicationNo. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981. 1]
-- When admin alone to anesthetized mice at concn of 100,000 ppm, CFC-21 induced arrhythmia and sensitized the heart to epinephrine. Tachycardia with hypotension was observed in both monkeys and dogs that were anesthetized and exposed at 50,000-100,000 ppm. Bronchoconstriction was noted at 25,000 ppm. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I,II, III. Cincinnati, OH: ACGIH, 1991. 434]**PEER REVIEWED**
-- /GUINEA PIGS/ ... EXPOSED /UP TO 2 HR/ @ CONCN OF 10.2% DIED &, ON AUTOPSY, CONGESTED LUNGS, CONGESTED KIDNEYS, CONGESTED LIVER, DISCOLORED SPLEEN, & HIGHLY CONTRACTED HEART WERE FOUND. [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values for Substances in Workroom Air. Third Edition, 1971. Cincinnati, Ohio: AmericanConference of Governmental Industrial Hygienists, 1971. (Plus supplements to 1979) 81]**PEER REVIEWED**
-- WHEN GUINEA PIGS WERE EXPOSED UP TO 2 HR ... @ CONCN RANGING FROM 1.2-10.2% BY VOL (12,000-102,000 PPM), CONCN OF 5.2% & HIGHER PRODUCED SIGNS OF IRRITATION, TREMORS, INCOORDINATION, & IRREGULAR BREATHING. [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values for Substances in Workroom Air. Third Edition, 1971. Cincinnati, Ohio: AmericanConference of Governmental Industrial Hygienists, 1971. (Plus supplements to 1979) 81]**PEER REVIEWED**
Ref: TOXNET profile from Hazardous Substances Data Base for Dichlorofluoromethane.
http://www.fluoridealert.org/pesticides/dichlorofluoromethan.toxnet.htm

Dichlorotetrafluoroethane (CFC-114) - Propellant, Former EPA List 2 Inert - CAS No. 76-14-2

-- The American Conference of Governmental Industrial Hygienists (ACGIH) has assigned dichlorotetrafluoroethane a threshold limit value (TLV) of 1000 ppm (6990 mg/m(3)) as a TWA for a normal 8-hour workday and a 40-hour workweek [ACGIH 1994, p. 19].
-- Rationale for Limits: The NIOSH limit is based on the risk of respiratory irritation, asphyxia at high concentrations [NIOSH 1992]. The ACGIH limit is based on the risk of systemic toxicity and cardiac sensitization [ACGIH 1991, p. 444].
-- Effects on Animals: dichlorotetrafluoroethane is a cardiac sensitizer, an asphyxiant, and a weak narcotic at extremely high concentrations [ACGIH 1991]. Dogs exposed to 200,000 ppm of dichlorotetrafluoroethane for 16 hours died, but exposures at this level for 8 hours caused tremor and convulsions [Hathaway et al. 1991]. Serious arrhythmia occurred in one of 12 dogs exposed once to 25,000 ppm of dichlorotetrafluoroethane and given intravenous epinephrine. Dichlorotetrafluoroethane is reported to reduce pulmonary compliance and act as a bronchoconstrictor [ACGIH 1991]. Guinea pigs exposed to a dichlorotetrafluoroethane concentration of 47,000 ppm developed respiratory irritation [Hathaway et al. 1991].
Ref: US OSHA (Occupational Safety & Health Administration, U.S. Department of Labor).
http://www.osha-slc.gov/SLTC/healthguidelines/dichlorotetrafluoroethane/recognition.html

Diflufenzopyr - Herbicide - CAS No. 109293-97-2

Subschronic toxicity: Histopathological findings were an increased incidence of foamy macrophages in the lungs in the 10,000 and 20,000 ppm groups, both sexes, and testicular atrophy in the 20,000 ppm group. Following the 47-week recovery period, the only treatment-related effects which showed partial or no evidence of recovery were foamy macrophages in the lungs and testicular atrophy.
Ref: Federal Register: December 12, 2001 [Page 64257-64262]. Notice of Filing a Pesticide Petition to Establish a Tolerance for a Certain Pesticide Chemical in or on Food.
http://www.fluoridealert.org/pesticides/Diflufenzopyr.FR.Dec12.2001.htm

Dithiopyr - Herbicide - CAS No. 97886-45-8

The following results were presented by a Monsanto scientist.
-- Thirteen-week Feeding Study in Rats. Dithiopyr was administered via the diet to groups of 12 male and 12 female F-344 rats for 13 weeks at concentrations of 0, 10, 100, 1000 and 5000 ppm.. Other findings included [no concentrations listed] multiple organ weight effects, thyroid follicular hypertrophy, adrenal cortical hypertrophy, and pulmonary foam cell aggregation. The subchronic NOEL in rats is considered to be 10 ppm. (The Institute of Environmental Toxicology, 1988)
Ref: Summary of Toxicology Studies With Dithiopyr. Dennis P. WARD. Toxicology Department, The Agricultural Grop, A Unit of Monsanto Company (Received February 20, 1993). Also available at
http://wwwsoc.nii.ac.jp/pssj2/tec_info/dithiopy.pdf

Fipronil - Acaracide, Insecticide - CAS No. 120068-37-3

The rat chronic/carcinogenicity study was negative for carcinogenicity. The LOAEL for females was 0.5 ppm (0.032 mg/kg/day), based on clinical signs of toxicity. There was no NOEL established. For males, the NOAEL was 2 ppm (0.098 mg/kg/day), based on clinical signs of toxicity, and stomach and lung histopathology at 10 ppm (0.497 mg/kg/day).
Ref: August 24, 2005. Federal Register. Fipronil; Notice of Filing a Pesticide Petition to Establish a Tolerance for a Certain Pesticide Chemical in or on Food.
http://www.fluorideaction.org/pesticides/fipronil.fr.aug.24.2005.html

Flonicamid - Insecticide - CAS No. 158062-67-0

Suggestive Evidence of Carcinogenicity, but not sufficient to assess human carcinogenic potential. Nasal lacrimal duct squamous cell carcinomas possibly treatment-related in female Wistar rats; Mitogenesis MOA accepted for lung tumors in CD-1 mice (both sexes).
Ref: April 26, 2006 . Chemicals Evaluated for Carcinogenic Potential by the Office of Pesticide Programs. From: Jess Rowland, Chief Science Information Management Branch Health Effect Division (7509C) Office of Pesticide Programs, USEPA.
http://www.fluorideaction.org/pesticides/pesticides.cancer.potential.2006.pdf

-- In the 18-month mouse study... There were statistically significant increases in the incidence of alveolar/bronchiolar adenomas in both sexes of treated groups with hyperplasia/hypertrophy of epithelial cells in terminal bronchioles. There was a statistically significant increase in the incidence of alveolar/bronchiolar carcinomas in males at 750 ppm and 2,250 ppm and in females at 2,250 ppm only. These effects in the lungs of mice were not life threatening as most of effects were observed at the terminal sacrifice and there was no effect of treatment on mortality in the study. A NOAEL could not be determined from the dose levels administered. Mechanism-of-action studies have indicated that the lung effects are unique to the mouse and are not likely to translate to other species including the rat. Flonicamid technical was not carcinogenic in the rat.
Ref: Federal Register: May 23, 2003 (Volume 68, Number 100)] [Notices] [Page 28218-28222]. Flonicamid; Notice of Filing a Pesticide Petition to Establish a Tolerance for a Certain Pesticide Chemical in or on Food.
http://www.fluorideaction.org/pesticides/Flonicamid.FR.May23.2003.htm

A second 18-month mouse study was conducted in CD-1 mice at dose levels ranging from 10 to 250 ppm to establish a NOAEL for hyperplasia/hypertrophy of epithelial cells in terminal bronchioles and for the incidence of alveolar/bronchiolar adenomas and carcinomas in both sexes. There was a statistically significant increase in the incidence of alveolar/bronchiolar adenomas in males at 250 ppm. In females, there was no statistically significant increase in the incidence of pulmonary neoplastic lesions at any dose level. The incidence of hyperplasia/hypertrophy of epithelial cells lining the terminal bronchioles of the lungs was statistically increased at 250 ppm in both sexes. There were no treatment-related increases in neoplastic or non-neoplastic lesions at dose levels of 80 ppm or lower in either sex. The NOAEL was 80 ppm, equivalent to 10.0 and 11.8 mg/kg body weight/day for males and females, respectively. This study confirmed a threshold for these effects at 80 ppm, which had been indicated in studies on the mechanism.
Ref: Federal Register. Jully 7, 2004. Flonicamid; Notice of Filing a Pesticide Petition to Establish a Tolerance for a Certain Pesticide Chemical in or on Food. [OPP-2004-0132; FRL-7362-5].
http://www.fluoridealert.org/pesticides/flonicamid.fr.july7.2004.htm

-- Carcinogenicity (mice). NOAEL was not established. LOAEL is 250 ppm (equivalent to 29/38mg/kg/ day [M/F]), based on minimal to moderate centrilobular hepatocellular hypertrophy, minimal to severe extramedullary hematopoiesis, minimal to moderate pigment deposition in the sternal bone marrow, and increased incidence of tissue masses/nodules in the lungs in the males, and minimal to moderate decreased cellularity in the femoral bone marrow and hyperplasia/hypertrophy of the epithelial cells of the terminal bronchioles of the females. At the doses tested, the carcinogenic potential of IKI-220 (flonicamid) is positive at 250 ppm in males and females based on the increased incidence of alveolar/bronchiolar adenomas, carcinomas, and combined adenomas/carcinomas. Dosing was considered adequate based on increased incidence of tissue masses/nodules in the lungs and microscopic findings in the liver, spleen, bone marrow, and lungs. However, data were provided suggesting this effect is specific to sensitive strains of mice. Carcinogenic in mice.
-- Carcinogenicity (mice). NOAEL is 80 ppm (equivalent to 10/12 mg/kg/day in males/females). LOAEL is 250 ppm (equivalent to 30/36mg/kg/day in males/females) based on lung masses and terminal bronchiole epithelial cellhyperplasia/ hypertrophy in both sexes. At the doses tested, the carcinogenic potential of IKI-220 (flonicamid) is positive in males and females based on the incidences of alveolar/ bronchiolar adenomas, carcinomas,and combined adenomas and/or carcinomas. Dosing was considered adequate based on lung masses and terminal bronchiole epithelialcell hyperplasia/ hypertrophy in both sexes. Carcinogenic in mice.
Ref: August 31, 2005. Flonicamid; Pesticide Tolerance. Final Rule. Federal Register.
http://www.fluoridealert.org/pesticides/flonicamid.fr.aug.31.2005.html

-- 52964 - 0068, 0069 & 0070 216042, 216043, 216044 “Vol 0068: Dietary Carcinogenicity of IKI-220 Technical in Mice; Vol 0069: Pathology Sub-Report (Supplemental) for Dietary Carcinogenicity of IKI220 Technical in Mice; Vol 0070: Historical Data for Dietary Carcinogenicity of IKI-220 Technical in Mice,” (Nagaoka, T., Nakashima, N.; Shin Nippon Biomedical Laboratories, Ltd., Kagoshima, Japan; The Institute of Environmental Toxicology, Ibaraki, Japan; 1/22/04, 3/30/04, 1/22/04 for volumes 0068, 0069 & 0070, respectively). Flonicamid technical (IKI-220: 98.7% pure) was fed in diet to Charles River Crj:CD-1®(ICR)BR mice (50/sex/dose) at 0, 10, 25, 80 and 250 ppm (equivalent doses: M = 1.20, 3.14, 10, 30.3 mg/kg/day; F = 1.42, 3.67, 11.8, 36.3 mg/kg/day) for 78 weeks. Systemic NOEL = 80 ppm (There was an increase in lung hyperplasia and hypertrophy (both sexes) and liver fatty change in centrilobular hepatocytes (F) at 250 ppm. There was a statistically significant decrease in absolute kidney weights in females at 250 ppm. There was a statistically significant increase in lung masses--pulmonary adenomas and carcinomas in males at 250 ppm.) Not acceptable (There were numerous deficiencies in this study (see A., above). There were no interim kills, nor were all target organs examined and weighed as recommended by FIFRA Guidelines.), not upgradeable. Possible adverse effect indicated (There was a statistically significant increase in pulmonary adenomas and carcinomas in males at 250 ppm. Silva, 4/29/05.
Reference: April 28, 2005 - Summary of toxicology data. California EPA, Department of Pesticide Regulation, Medical Toxicology Branch.
http://www.fluorideaction.org/pesticides/flonicamid.ca.epa.2005.pdf

Fluazifop-P-butyl - Herbicide - CAS No. 79241-46-6

Acute Toxicity ... Breathing small amounts of the product Fusilade 2000 may cause vomiting and severe lung congestion; larger amounts may ultimately lead to labored breathing, coma, and death [37].
Ref: EXTOXNET. Pesticide Information Profile for Fluazifop-p-butyl. Cornell University.
http://ace.ace.orst.edu/info/extoxnet/pips/fluazifo.htm

Fluazinam - Fungicide - CAS No. 79622-59-6

In subchronic and chronic toxicity studies, fluazinam targeted the following organs: liver, lung, uterus, testes, pancreas, thymus, thyroid, stomach, eyes and brain...
Ref: Canada: Regulatory Note REG2003-12. Fluazinam. Pest Management Regulatory Agency. Health Canada. Ottawa. October 27, 2003.
http://www.fluorideaction.org/pesticides/fluazinam.canada.report2003.pdf

PubMed Abstract: We report two cases of occupational asthma caused by sensitisation to powdered fungicides fluazinam and chlorothalonil, from the same fungicide formulation plant. Both developed work related lower respiratory symptoms after a latent interval of asymptomatic exposure. The diagnosis in each case was confirmed with a serial peak flow record in the workplace followed by specific inhalation tests. These fungicides are known to cause dermatitis; this report indicates that these compounds can induce specific immunological reactions in the airways as well as skin.
Ref: Occup Environ Med 2003 Jan;60(1):76-7. Occupational asthma from fungicides fluazinam and chlorothalonil; by Draper A, Cullinan P, Campbell C, Jones M, Newman Taylor A.

-- Subchronic toxicity. The NOAEL for the 13 week feeding study in rats was 50 ppm (4.1 mg/kg/day). The LOAEL was 500 ppm (41 mg/kg/day), based on periacinar hepatocellular hypertrophy and sinusoidal chronic inflammation in males, increased liver weights in males and increased lung weights in females.
-- Chronic toxicity. Fluazinam was not carcinogenic in rats. A NOAEL of 10 ppm (0.43 mg/kg/day) of fluazinam was established based on the following effects at 1,000 and/or 100 ppm: lower food consumption and efficiency of food utilization, slight anemia, elevated cholesterol, increased liver weights, an increased number of macroscopic liver and testes lesions and an increased incidence of microscopically observed lung, liver, pancreas, lymph node and testes lesions.
Ref: Federal Register: December 6, 2000 [Page 76253-76258]. Notice of Filing Pesticide Petitions to Establish and to Extend Tolerances for Certain Pesticide Chemicals in or on Food.
http://www.fluoridealert.org/pesticides/Fluazinam.FR.December.2000.htm

Flucythrinate - Acaricide, Insecticide - CAS No. 70124-77-5

-- Groups of 6 male and 6 female Beagle dogs received technical flucythrinate (87.3% pure) in the diet at 0, 30, 100, or 300 ppm daily for 24 months... At sacrifice, the relative liver, kidney, and pituitary weights were increased in both high-dose males and females, while increases in relative spleen, testis and lung weights were noted for high-dose males only... Upon histological examination, mid- and high-dose groups exhibited increased evidence of interstitial pneumonia, compared to controls... ((Spicer et al., 1984).
Ref: 1985 World Health Organization Review for Flucythrinate.
http://www.fluoridealert.org/pesticides/Flucythrinate.1985.WHO.htm

Fluometuron - Herbicide - CAS No. 2164-17-2

Group C -- Possible Human Carcinogen. Statistically significant increases in combined adenomas/carcinomas of the lung (M); Malignant lymphocytic lymphomas (F); CD-1 mice.
Ref: April 26, 2006 . Chemicals Evaluated for Carcinogenic Potential by the Office of Pesticide Programs. From: Jess Rowland, Chief Science Information Management Branch Health Effect Division (7509C) Office of Pesticide Programs, USEPA.
http://www.fluorideaction.org/pesticides/pesticides.cancer.potential.2006.pdf

• A re-examination and statistical analysis of the rates of all lymphocytic lymphomas in female mice and all alveolarhronchiolar hyperplasia, adenomas, and carcinomas in male mice from the carcinogenicity study in mice (0, 10,500, or 2000 ppm [83-2b]) indicated that male mice had a significant increasing trend in alveolar/bronchiolar adenomas andor carcinomas combined at p < 0.05. There were no significant differences in the pair-wise comparisons of the dosed groups with the controls. The male alveolarhonchiolar tumor rates were 15/56, 16/59, 19/56, and 24/58, respectively (L. Taylor Memorandum 9/13/95, TXR 012742). Female mice had a significant increasing trend and a significant difference in pair-wise comparison of the high-dose group (2000 ppm) with the controls for lymphocytic lymphomas at p < 0.05. The lymphatic tissue tumor rates were 4/5 1, 10124, 6/17, and 12/53, respectively (L. Taylor Memorandum 9/13/95, TXR 012742).(page 9)
• D. Classification of Carcinogenic Potential. The Health Effects Division Carcinogenicity Peer Review Committee (CPRC) met on Oct. 11, 1995 to discuss and evaluate the weight-of-the-evidence on fluometuron with particular reference to its carcinogenic potential. The consensus of the CPRC was that fluometuron should be classified as Group C -possible human carcinogen and for the purpose of risk characterization, both a low dose extrapolation model (Q,’) applied to the animal data (lung tumors in male mice) and the Reference Dose (RfD) approach should be used. This was based on statistically significant increases in combined adenomadcarcinomas of the lungs in male mice and malignant lymphocytic lymphomas in female mice, at a dose which was less than adequate for fully assessing the carcinogenic potential of fluometuron ( L. Taylor Memorandum 8/28/96, TXR 012049).
A quantitative risk assessment-Q,* was performed for fluometuron (B. Fisher Memorandum 12/24/96, TXR 012809). The unit risk, QI*(mg/kg/day)-’of fluometuron, based upon male mouse combined lung (adenomas and/or carcinomas) tumor rates is 1.80 x lo-*in human equivalents (converted from animals to humans by use of the 314‘s scaling factor-1994, Tox Risk, 3.5-K. Crump) (Ref. 1). The dose levels used from this 2-year study were 0, 10,500, and 2000 ppm of fluometuron. The corresponding tumor rates (from re-read slide data, 7/92) for the male mice were 15/56, 16/59, 19/56, and 24/58 respectively.
The estimate of unit risk, Q1*was based upon lung (adenoma and/or carcinoma) tumor rates in male mice. Since male mice had statistically significant increases in mortality with dose increments of fluometuron, the estimate of the unit risk, Q1*,was obtained by the application of the time-to-tumor Weibull model (Tox-Risk program, version 3.5-K. Cnunp). The resulting estimate of unit risk, Q1*,was converted to human equivalents by the use of weights of 0.03 kg for the mice and 70 kg for the humans and the 3/4’s scaling factor for interspecies extrapolation. It is to be noted that Q,* (mg/kg/day)-’ is an estimate of the upper bound on risk and that (as stated in the EPA Risk Assessment Guidelines) “the true value of the risk is unknown, and may be as low as zero. (page 11-12).
(1). See memo-Deriving Q,*s Using the Unified Interspecies Scaling Factor, P.A. Fenner-Crisp. Director-HED, 7/1/94.
Ref. February 1, 2005. US EPA: Fluometuron: Revised HED Risk Assessment for Phase III of the Reregistration Eligibility Decision. Docket Identification Number: OPP-2004-0372-0008. 
http://www.fluorideaction.org/pesticides/fluometuron.opp-2004-0372-0008.pdf

Fluorapatite - US EPA Inert - CAS No. 1306-05-4

Abstract: In a study of the effects of phosphorite and apatite (1306-05-4) dusts on respiratory function, industrial hygiene monitoring of workplace total and respirable dusts was performed on a cohort of 118 males, mean age 37.3 years, who had been employed in processing phosphorite and apatite ores for a mean of 8.6 years. The comparisons consisted of 149 healthy males, mean age 35.6 years, who had never been exposed to phosphorite or apatite dusts. Approximately 67% of the subjects in each group were smokers. The subjects completed a respiratory symptom questionnaire, pulmonary function testing was performed, and chest X-rays were obtained. Total workplace dust concentrations ranged from 14 to 228 milligrams per cubic meter. The respirable fraction accounted for approximately 18% of the total dust concentrations and consisted primarily of calcium-oxide (1305788), phosphorus oxides, silica (14808607), and fluorides. Both the cohort and comparisons reported similar prevalences of chronic cough, excess sputum production, and dyspnea, 15 and 12%, respectively. The chest X-ray films of both groups were similar. Group mean values of forced vital capacity (FVC), 1 second forced expiratory volume (FEV1), and maximum expiratory flow at 25% (MEF25) and 75% of FVC (MEF75) were significantly lower in nonsmoking phosphorite and apatite workers than in nonsmoking comparisons. Mean transit times (MTTs) were significantly longer in the nonsmoking exposed workers than in nonsmoking comparisons. These changes were not significantly associated with duration of phosphorite or apatite exposure. FVC, FEV1, MEF25, maximum expiratory flow at 50% FVC, MEF75, and MTT were significantly decreased in smoking comparisons relative to smokers in the cohort. No smoking related changes in these parameters were seen in the exposed workers. The authors conclude that occupational exposure to phosphorite and apatite dusts causes decrements in pulmonary function in nonsmoking workers.
Ref: Assessment of the Respiratory System in Workers Occupationally Exposed to Phosphorite and Apatite Dusts; by Mikulski T, Podraza H, Steciuk W, Swiech Z . International Journal of Occupational Medicine and Environmental Health, Vol. 7, No. 2, pages 119-124, 20 references, 1994.

Abstract: Fifty mg of apatite-concentrate and apatite-nepheline (apatite ore), suspended in 1 ml of physiological saline solution, were applied once intratracheally to female albino rats. Twenty-six, 39 and 52 wk later the animals were sacrificed and a histological examination of the macroscopically affected parts of the lungs and the paratracheal lymph nodes was done. In all 52 wk animals a histocytical and fibrocytical formation of nodules in the lungs with a desquamation of the epithelia and metaplastic modifications of the plateepithelium of the bronchial mucous membrane was observed. Application of apatite-concentrate resulted in a lympho-plasmacellular reaction with subsequent leucocytical infiltration. In both dust samples the examined lymph nodules showed the symptoms of a chronic lymphadenitis. Apatite-ore causes a fibrous injury of the parenchyma of the lungs. This damage was not observed in the case of apatite-concentrate.
CAS Registry Numbers:
1302-72-3 - Nepheline: (Na, K)AlSiO4 , Sodium Potassium Aluminum Silicate
1306-05-4 - Fluorapatite
Ref: (Investigation on the effects of a singly intratracheal application of apatite-nepheline and apatite-concentrate dust to rat lungs.) by HOLLENBACH K, KERSTEN E, PATZELT K, SCHWESINGER G. INT ARCH ARBEITSMED; 28 (3). 1971 271-282

Abstract: The prevalence of pneumoconioses among phosphate (1306-05-4) rock workers in Brazil was assessed. The 73 workers evaluated in the investigation were exposed to phosphate rock extracted in the states of Goias and Minas Gerais, where the material was crushed and then transported to Paulinia for storage in underground mills. Subjects submitted to a detailed respiratory questionnaire, a physical examination emphasizing the respiratory system, pulmonary function tests, chest x-rays, and, in two cases, lung biopsies through thoracotomy. The quantity of free silica (7631869) in airborne samples was measured by colorimetric analysis. A semiquantitative analysis was performed on airborne samples using x-ray spectrometry. Twenty of the workers were noted to have pneumoconioses. Mean exposure was 46 months. The majority of the cases had no respiratory symptoms. No significant fibrosis was noted, and no pleura disease or mediastinal alterations were observed. No traces of free silica were detected by diffraction analysis. The author concludes that the high prevalence of pneumoconioses noted in this study must derive from the particularly poor working conditions at the facilities. A regular followup using lung function tests and chest x-rays should be included in the routine examination of phosphate rock workers.
Ref: Prevalence of Pneumoconioses among Phosphate Rock Workers in Brazil by de Capitani EM. Proceedings of the VIIth International Pneumoconioses Conference, Part II. Pittsburgh, Pennsylvania, August 23-26, 1988. NIOSH, U.S. Department of Health and Human Services, DHHS (NIOSH) Publication No. 90-108 Part II, pages 1310-1311, 1990.

Abstract: The pulmonary nonasbestos mineral fiber content was analyzed in the lungs of 20 individuals who had no occupational exposure to fibers. Thirteen different mineral species were identified which accounted for 71 percent of the fibers counted. Among those found were apatite (1306-05-4), talc (14807966), attapulgite (1337764), gypsum (13397245), silica (7631869), rutile (13463677), kaolinite (1318747), mullite (1302767), illite (12173603), pyroxene (12174377), pyrophyllite (68136618), feldspar, vermiculite (1318009), and chlorite (1318598). The average number of nonasbestos fibers for the 20 cases was 106,000/gram wet lung. There was no significant difference recorded between smokers and nonsmokers nor was there a difference based on age. Apatite was the most frequently observed fiber with a mean of 19,000 fibers/gram wet lung, or 18 percent of the nonasbestos fibers present. Talc was the next highest in concentration and together talc and apatite constituted over one third of the total fibers present. Only silica was found in every lung sample. Eighty six percent of the fibers were between 1 and 4.9 microns in length with 3 percent being over 10 microns in length. Concerning distribution in the lungs, the mean number of fibers in the subpleural upper lobe was 30,500; in the peripheral lower lobe 37,000; in the central upper lobe 19,500; and in the central lower lobe 19,500 fibers/gram wet lung. Interstitial fibrosis did not occur in any patient unless it was explainable as a result of treatment or old infectious disease. Three of these individuals had lung cancer and one had gastrointestinal cancer but in none of these individuals were there any differences in nonasbestos fiber content in the lungs when compared to other members of the study group.
Ref: Nonasbestos Pulmonary Mineral Fibers in the General Population by Churg A. Environmental Research, Vol. 31, No. 1, pages 189-200, 22 references, 1983.

Abstract: Small-airway lesions were identified in histologic sections from the lungs of 7 workers with histories of exposure to nonasbestos dusts. The lesions consisted of deposits of fibrous tissue, often accompanied by pigment, in the walls of membranous and respiratory bronchioles and alveolar ducts. Comparison with a matched population of persons with no dust exposure revealed that the changes in the respiratory bronchioles and alveolar ducts were morphologically distinctive and could be used to diagnose the lesions. Structurally, these lesions were similar to those described in the airways of asbestos workers, although comparison with the authors' previous results indicated that the number of severely affected airways was less in the nonasbestos dust group. Mineralogic analysis indicated that these abnormalities were produced by a variety of different dusts including silica, iron oxide and aluminum oxide, and that occult asbestos exposure, although possible in 3 cases, was most likely not a primary cause of disease. This lesion, called mineral dust airways disease, was a nonspecific reaction of the small airways to inorganic particulates. The presence of such changes cast doubt on the theory that small-airway abnormalities in asbestos workers were the earliest form of asbestosis.
CAS Registry Numbers:
17068-78-9 - Anthophyllite asbestos
14567-73-8 - Tremolite
12172-73-5 - Asbestos, amosite
12001-28-4 - Asbestos, crocidolite
12001-26-2 - Mica
7631-86-9 - Siliceous earth, purified
1344-28-1 - Aluminum oxide
1318-74-7 - Kaolinite (Al2(OH)4(Si2O5))
1317-80-2 - Rutile (TiO2)
1306-05-4 - Fluorapatite
Ref: Small-airway lesions in patients exposed to nonasbestos mineral dusts. CHURG A, WRIGHT JL. HUM PATHOL; 14 (8). 1983. 688-693.

Abstract: Pure monoclinic or triclinic calcium pyrophosphate dihydrate (CPPD) crystals, apatite crystals or mixtures of these crystals were injected into the synovial-like space created by the rat air pouch to compare the acute inflammation induced by these crystals. Fluids were withdrawn 6 h after injection and examined for leukocyte counts, protease, prostaglandin E2 (PGE2) and tumor necrosis factor (TNF) levels. CPPD crystals (especially monoclinic CPPD) induced higher numbers of leukocytes, and more protease, PGE2 and TNF than apatite. CPPD seemed to play a predominant role in the acute inflammation induced by mixed crystals.
CAS Registry Numbers:
17031-92-4 - Diphosphoric acid, calcium salt (1:2), dihydrate
1306-05-4 - Fluorapatite
Ref: Comparison of the acute inflammation induced by calcium pyrophosphate dihydrate, apatite and mixed crystals in the rat air pouch model of a synovial space. WATANABE W, BAKER DG, SCHUMACHER H R JR. J RHEUMATOL; 19 (9). 1992. 1453-1457.

Fluorouracil - Former insect Chemosterilant; now used as a pharmaceutical - CAS No. 51-21-8

POTENTIAL ADVERSE EFFECTS ON FETUS: Exposure in first trimester resulted in skeletal abnormalities; hypoplasia of aorta, lungs, thymus, and gastrointestinal tract; and urinary tract abnormalities. Fetus exposed in third trimester had cyanosis and clonus.
Ref: TOXNET profile from Hazardous Substances Data Base.
http://www.fluoridealert.org/pesticides/Fluorouracil.TOXNET.HSDB.htm

Gliftor - Rodenticide - Rodenticide - CAS No. 8065-71-2

Abstract. The single administration of gliftor (I; internally, 40-160 mg/kg) caused considerable destructive changes and circulatory disorders in the internal organs of rats. The maximum tolerance dose of I (60 mg/kg) caused hyperplasia of the cells of the RES in the spleen, proliferation of local cells, and inflammatory cellular infiltration of the alveolar walls in the lungs.
Ref: Morphological changes of internal organs of experimental animals after oral administration of gliftor; by KNYSH VS, TKACH NZ, TSAREVSKII LP. TR INST KRAEV PATOL AKAD NAUK KAZ SSR; 22 1971 28-30. [Abstract from Toxline at Toxnet.]

Abstract. Rats were subjected to the single inhalation effect of vapors of the zoocide gliftor (I; 50, 100, 350, 520, and 1100 mg/m-3). Morphological changes were noted beginning with a concentration of 350 mg/m-3. In a chronic experiment (4 mo.) the rats were subjected to I poisoning in a concentration of 10, 13, 64, and 110 mg/m-3. Distinct morphological changes in the organs were noted under the effect of concentrations 64 and 110 mg/m-3. Under the chronic effect of I there were considerable circulatory disorders and destructive changes of the interanl organs, especially in the liver, lungs, spleen, and kidneys.
Ref: Pathomorphological changes in internal organs of white rats under the inhalation effect of gliftor; by KNYSH VS, TKACH NZ, TSAREVSKII LP, MILOVANOVA VI. TR INST KRAEV PATOL AKAD NAUK KAZ SSR; 22 1971 23-28. [Abstract from Toxline at Toxnet.

Hydramethylnon - Insecticide - CAS No. 67485-29-4

Group C -- Possible Human Carcinogen. Lung adenomas & combined adenomas/carcinomas; CD-1 mice (F).
Ref: April 26, 2006 . Chemicals Evaluated for Carcinogenic Potential by the Office of Pesticide Programs. From: Jess Rowland, Chief Science Information Management Branch Health Effect Division (7509C) Office of Pesticide Programs, USEPA.
http://www.fluorideaction.org/pesticides/pesticides.cancer.potential.2006.pdf

The Cancer Peer Review Committee determined that hydramethylnon should be classified as a Group C carcinogen, a possible human carcinogen, and recommended that, for the purpose of risk characterization, the Reference Dose approach should be used for quantification of human risk. This classification was based upon statistically significant increases in lung adenomas at 50 and 100 ppm (27% and 27%, respectively) and combined lung adenomas/carcinomas at 25, 50, and 100 ppm (32%, 40%, and 35%, respectively) in female mice. The MTD is between 50 ppm and 100 ppm in both sexes of mice.
Ref: US EPA. Reregistration Eligibility Decision (RED) Hydramethylnon. EPA 738-R-98-023. December 1998.
http://www.fluoridealert.org/pesticides/hydramethylnon.red.1998.pdf

Indoxacarb - Insecticide - CAS No. 173584-44-6

-- There was possible evidence of lung damage in the acute inhalation studies with both DPXMP062 and DPX-JW062. “Lung noise,” observed with JW062 may indicate the development of acute lung injury and high permeability pulmonary edema. This was not unexpected since an oxidant was generated during indoxacarb metabolism. “Hunched over back and gasping” were also present and suggested arterial hypoxemia that accompanies alveolar flooding. The acute inhalation study report with indoxacarb 70% manufacturing use product, noted that a “red nasal discharge” was detected for 2 days after exposure. This may be indicative of a lung exudate, a sign of lung injury.
Ref: USEPA. May 23, 2007. Indoxacarb. Health Effects Division (HED) Risk Assessment for Grapes; Vegetable, Brassica, Leafy, Group 5; Turnip Greens; Vegetable, Leafy, Except Brassica (Group 4); Pome Fruits (Group 11, except pear); Tuberous and Corm Vegetables (Subgroup 1C); Cucurbit Vegetables (Group 9); Stone Fruits (Group 12); Cranberry; Mint; Okra; Southern Pea; and Fire Ant Bait.
http://www.fluoridealert.org/pesticides/EPA-HQ-OPP-2005-0149-0005.pdf

Nissol (also known as MNFA or MNAF) - Acaricide, Insecticide - CAS NO. 5903-13-9

TOXICITY Ref: ChemIDplus for Nissol. Available at Toxnet.
Organism	Test Type	Route	Reported Dose (Normalized Dose)	Effect	Source
guinea pig	LD50	skin	5mg/kg (5 mg/kg)	LUNGS, THORAX, OR RESPIRATION: DYSPNEA	Toxicology and Applied Pharmacology. Vol. 12, Pg. 536, 1968.
guinea pig	LDLo	subcutaneous	1mg/kg (1 mg/kg)	LUNGS, THORAX, OR RESPIRATION: DYSPNEA	Toxicology and Applied Pharmacology. Vol. 12, Pg. 536, 1968.
mouse	LD50	intraperitoneal	164mg/kg (164 mg/kg)	LUNGS, THORAX, OR RESPIRATION: RESPIRATORY DEPRESSION	Toxicology and Applied Pharmacology. Vol. 12, Pg. 536, 1968.
mouse	LD50	subcutaneous	216mg/kg (216 mg/kg)	LUNGS, THORAX, OR RESPIRATION: RESPIRATORY DEPRESSION	Toxicology and Applied Pharmacology. Vol. 12, Pg. 536, 1968.
rabbit	LD50	oral	1500ug/kg (1.5 mg/kg)	LUNGS, THORAX, OR RESPIRATION: OTHER CHANGES	Experimental Animals. Jikken Dobutso Iho. Vol. 21, Pg. 88, 1972.
rabbit	LDLo	intravenous	5mg/kg (5 mg/kg)	LUNGS, THORAX, OR RESPIRATION: DYSPNEA	Toxicology and Applied Pharmacology. Vol. 12, Pg. 536, 1968.
rat	LD50	subcutaneous	41mg/kg (41 mg/kg)	LUNGS, THORAX, OR RESPIRATION: RESPIRATORY DEPRESSION	Toxicology and Applied Pharmacology. Vol. 12, Pg. 536, 1968.

Noviflumuron - Insecticide - CAS No. 121451-02-3

“XDE-007: 18-Month Oncogenicity Study in CD-1 Mice,” (Johnson, K.A.; Toxicology & Environmental Research and Consulting, The Dow Chemical Company, Midland, MI; 4/25/05). XDE-007 technical (N-[3,5-dichloro-2-fluoro-4-(1,1,2,3,3,3hexafluoropropoxy)phenyl]-N’-(2,6-difluorobenzoyl)urea), 97.9% pure) was fed in diet to CD-1 mice (50/sex/dose) at 0, 0.5, 3 (males only), 30 and 100 (females only) mg/kg/day for up to 18 months. Systemic NOEL = 3 mg/kg/day (males) and 30 mg/kg/day (females)... There was an increased incidence in evidence of inflammation in lung in both sexes at the high dose... Females showed an increased incidence in lung carcinomas (non-metastatic) at 100 mg/kg/day (0, 0, 1, 2** by Peto’s statistics).
Ref: August 2005 - Summary of toxicological data. California EPA, Department of Pesticide Regulation, Medical Toxicology Branch.
http://www.fluorideaction.org/pesticides/noviflumuron.ca.epa.2005.pdf

Poly(difluoromethylene), alpha-chloro-omega-(2,2-dichloro-1,1,2- trifluoroethyl) - EPA List 3 Inert - CAS No. 79070-11-4

-- Inhalation of the decomposition products of Poly TFE may cause polymer fume fever; a lung irritation requiring medical treatment for fluorine compounds which can cause delayed pulmonary edema. A polymer fume fever is a flu-like condition which occurs several hours after exposure and subsides within 24 hours even in the absence of treatment. Polymer fume fever does not cause permanent injury and the effects are not cumulative.
-- Human health effects of overexposure by inhalation to very high concentrations may cause temporary alteration of the heart's electrical activity with irregular pulse, palpitations, or inadequate circulation. Individuals with preexisting diseases of the central nervous or cardiovascular system may have increased susceptibility to the toxicity of excessive exposures.
Ref: Material Safety Data Sheet for: VDX Dry Lubricant
Prepared: Sat Apr 05 2003. Also available at:
http://www.microcare.com/MSDS/MSDS-VDX.US.phtml
Manufacturer: Micro Care Corporation, 595 John Downey Drive, New Britain, CT. 06051 USA

Potassium bifluoride - Wood Preservative - CAS No. 7789-29-9

Ingestion: May cause osseous fluorosis (increased radiographic density of the bones). May cause kidney damage, asthma and symptoms resembling rheumatism. Target Organ Effects: Chronic ingestion may cause kidney damage.
Ref: Material Safety Data Sheet for Potassium Hydrogendifluoride [synonym]. LA-CO INDUSTRIES, Inc./Markal Co. Product Name: SILVER BRAZING FLUX PASTE Revision #: 1.5 Date Prepared: March 1, 1995. Date Revised: August 6, 2002.
http://www.fluorideaction.org/pesticides/potassium.bifluoride.msds.pdf

Pyridalyl - Insecticide - CAS No. 179101-81-6

Subchronic toxicity.
-- Pyridalyl technical was tested in rats in a 3-month feeding study. Effects included decreased body weight gain, altered blood biochemistry, increased relative liver weight and histopathological changes in the liver, ovary, adrenal and lung. The NOAEL is 100 ppm (5.56 mg/kg/day in males and 6.45 mg/kg/day in females).
-- A 13-week oral (capsule) toxicity study was conducted in dogs. Effects included decreased body weight gain, clinical signs indicative of respiratory distress, hematological and blood biochemistry effects, increased liver, lung and kidney weights and histopathological alterations of the lung, kidney, adrenal and liver. The NOAEL was 10 mg/kg/day.
Ref: Federal Register: December 5, 2003. Pyridalyl; Notice of Filing a Pesticide Petition.
http://www.fluorideaction.org/pesticides/pyridalyl.fr.dec.5.2003.htm

Sodium fluorosilicate (Sodium Hexafluorosilicate) - Insecticiide, Wood Preservative, EPA List 3 Inert - CAS No. 16893-85-9

-- Toxicological Data. Human Data. Chronic exposure to sodium hexafluorosilicate dust at levels above the eight-hour TWA can result in severe calcification of the ribs, pelvis, and spinal column ligaments; effects on the enzyme system; pulmonary fibrosis; stiffness; irritation of the eyes, skin, and mucous membranes; weight loss; anorexia; anemia; cachexia; wasting; and dental effects. Long-term or repeated exposure to the skin can result in skin rash. A probable oral lethal dose of 50-500 mg/kg, classified as very toxic, has been reported for a 150-pound (70-kg) person receiving between 1 teaspoon and 1 ounce of sodium hexafluorosilicate. Cases of sodium hexafluorosilicate ingestion reported symptoms such as acute respiratory failure, ventricular tachycardia and fibrillation, hypocalcemia, facial numbness, diarrhea, tachycardia, enlarged liver, and cramps of the palms, feet, and legs.
-- -- Guinea pigs, 13- 55 mg/ m 3 (1.2- 7.2 ppm) in air for ¥ 6 h; Pulmonary irritation was observed. The lowest concentration that caused death when inhaled for 6 h was 33 mg/ m 3 . Patty (1963; cited by HSDB, 2000b)
-- -- Mice orally given sodium hexafluorosilicate (70 mg/kg; 0.37 mmol/kg) exhibited toxic effects in the peripheral nerves, sensation, and in behavior. In rats, an oral dose (248 mg/kg; 1.32 mmol/kg) administered intermittently for one month produced toxic effects in the kidney, ureter, and/or bladder, as well as musculoskeletal and biochemical effects (RTECS, 1997). Using guinea pigs, inhalation experiments (13-55 mg/m 3 [1.7-7.2 ppm] sodium hexafluorosilicate in air for ¥6 hours) resulted in pulmonary irritation; the lowest concentration that caused death was 33 mg/m 3 (4.3 ppm) (Patty, 1963; cited by HSDB, 2000b).
Ref: Sodium Hexafluorosilicate [CASRN 16893-85-9] and Fluorosilicic Acid [CASRN 16961-83-4]. Review of Toxicological Literature. October 2001. Prepared for Scott Masten, Ph.D. National Institute of Environmental Health Sciences P.O. Box 12233 Research Triangle Park, North Carolina 27709 Contract No. N01-ES-65402. Submitted by Karen E. Haneke, M.S. (Principal Investigator) Bonnie L. Carson, M.S. (Co-Principal Investigator) Integrated Laboratory Systems P.O. Box 13501 Research Triangle Park, North Carolina 27709.
http://www.fluoridealert.org/pesticides/fluorosilicates.nih.2001.pdf

Sulfuryl fluoride - Fumigant insecticide - CAS No. 2699-79-8

Ref: January 23, 2004. Sulfuryl Fluoride; Pesticide Tolerance. 40 CFR Part 180 [OPP-2003-0373; FRL-7342-1]. Final Rule. Federal Register
Excerpts from: Table 1.--Subchronic, Chronic, and Other Toxicity
Study Guideline	Type of Study	NOAEL mg/kg/day	LOAEL mg/kg/day	Based on:
None cited	2-Week inhalation study--rat	83/89 (M/F)	495/534 (M/F)	high mortality, decreased body weights, severe histopathology in the kidney, gross and histopathology in many tissues/ organs (secondary to kidney effects); severe inflammation of respiratory tissues in one survivor...
None cited	2-Week inhalation study--dog	26/27 (M/F)	79/80 (M/F)	intermittant tremors and tetany during exposure, minimal inflammatory changes in upper respiratory tract, decreased body weight (F only). Note: Increased serum fluoride at >= 26/27 mg/kg/day
None cited	2-Week inhalation study--rabbit	30/30 (M/F)	180/180 (M/F)	convulsions, hyperactivity, malacia (necrosis) in cerebrum, vacuolation of cerebrum, moderate inflammation of respiratory tissues
(870.3100)	90-Day inhalation toxicity--ra