Following upon yesterday’s bulletin, I would like to draw attention to another important and recent study from China.

The study was published in the December 2003 issue of the journal Environmental Geochemistry and Health. The authors of the study (Bo, et al) conducted an extensive analysis of the water fluoride concentrations in an area of Northeast China which suffers from an endemic skeletal fluorosis problem. Their conclusion?

“High fluoride (>1.0 mg L) in drinking water resulted in dental and skeletal fluorosis in local residents (children and pregnant women)… It has been determined that fluoride concentration in excess of 1.0 mg L exposes residents to high health risks based on risk identification.”

This conclusion – that skeletal fluorosis resulted from drinking water containing in excess of 1 ppm fluoride – is consistent with the experience elsewhere in China. Indeed, according to the Chinese drinking water standard (GB5749-86), any water supply containing in excess of 1 ppm fluoride presents a risk for skeletal fluorosis.

To put this in perspective, the US EPA’s current Maximum Contaminant Level for fluoride in US drinking water supplies is 4 ppm. The EPA based this standard in part on the assumption that skeletal fluorosis was only found in communities in “other countries” with more than 10 ppm fluoride. In 1985, (when it wrote the MCL standard) the EPA stated:

“EPA notes that crippling skeletal fluorosis, rheumatic attack, pain and stiffness have been observed in a large number of individuals in other countries chronically exposed to fluoride in drinking water at levels of 10 mg/L to 40 mg/L” (Federal Register, Nov 14, 1985, p. 47144).

What’s striking about this statement, is not that it has been contradicted by more recent findings (such as this most recent study from China), but that it was contradicted before it was written by numerous, well-publicized, studies. For instance, in two of the most frequently cited papers on skeletal fluorosis in India, (Singh 1961, 1963) advanced fluorosis was observed at 1.2 ppm and between 1 and 2 ppm. Later, Siddiqui (1970) observed advanced fluorosis at 1.2-1.4 ppm, while Jolly (1970) reported skeletal fluorosis at 1.4 ppm. Additional studies reported skeletal fluorosis above 2 ppm, but far below the EPA’s estimated purported threshold of 10 ppm. This includes Pandit (1940); Siddiqui (1955); Kumar (1963); and Krishnamachari (1973) among others.

Meanwhile, more recent studies from Xu (1997) and Choubisa (2001) have documented skeletal fluorosis in China and India at 1.4 ppm. In addition, Xu reported 1 case of skeletal fluorosis in a community with 0.7 ppm.

It is therefore clear – based on the oldest, and newest evidence – that one of the key assumptions underpinning EPA’s current MCL of 4 ppm, was grossly incorrect.

Below, I have reprinted the abstract of the recent study from China (Bo 2003), and have listed the references for the other studies cited. I have also provided links of recent news articles discussing the impacts of skeletal fluorosis in both India and China.

Michael Connett
Editor, FAN Science Watch

———–

1) News Articles on Skeletal Fluorosis in India/China

————

2) Abstract of Recent Study Discussed Above

Environ Geochem Health. 2003 Dec;25(4):421-31.

Distribution and risk assessment of fluoride in drinking water in the west plain region of Jilin province, China.

Bo Z, Mei H, Yongsheng Z, Xueyu L, Xuelin Z, Jun D.
College of Environment and Resource, Jilin University, China.

The west plain region of Jilin province of northeast China is one of the typical endemic fluorosis areas caused by drinking water for many years. Investigations of hydrogeological and ecoenvironmental conditions as well as endemic fluorosis were conducted in 1998. Results show that the ground water, especially, the water in the unconfined aquifer is the main source of drinking water for local residents. The fluoride concentration in groundwater in the unconfined aquifers is higher than that in the confined aquifer in the west plain of Jilin province. The fluoride concentration in the unconfined aquifer can be used to classify the plain into fluoride deficient area, optimum area and excess area, which trend from west to east. High fluoride (>1.0 mg L(-1)) in drinking water resulted in dental and skeletal fluorosis in local residents (children and pregnant women). There exists a positive correlation between fluoride concentration in the drinking water and the morbidities of endemic fluorosis disease (r1 = 0.781, r2 = 0.872). Health risks associated with fluoride concentration in drinking water are assessed. It has been determined that fluoride concentration in excess of 1.0 mg L(-1) exposes residents to high health risks based on risk identification. The study area is classified into five health risk classes as shown in Figure 4. The risk indexes of this area more than 1.0 are accounted for 68% of the total west plain region.

PMID: 14740986 [PubMed – in process]

———-

3) References:

Bo Z, et al. (2003). Distribution and risk assessment of fluoride in drinking water in the West Plain region of Jilin Province, China.Environmental Geochemistry and Health 25: 421-431.

Choubisa SL, et al. (2001). Endemic fluorosis in Rajasthan. Indian Journal of Environmental Health 43: 177-89.

Jolly SS. (1970). Hydric fluorosis in Punjab (India). In: Vischer TL. Fluoride in Medicine. Hans Huber: Switzerland. pp. 106-121.

Krishnamachari KA, Krishnaswamy K. (1973). Genu valgum and osteoporosis in an area of endemic fluorosis. The Lancet 2: 877-879.

Kumar SP, Harper RA. (1963). Fluorosis in Aden. British Journal of Radiology 36: 497-502.

Pandit CG, et al. (1940). Endemic fluorosis in South India. Indian Journal of Medical Research 28: 533-558.

Siddiqui AH. (1970). Neurological complications of skeletal fluorosis with special reference to lesions in the cervical region. Fluoride3: 91-96.

Siddiqui AH. (1955). Fluorosis in Nalgonda District, Hyderabad-Deccan. British Medical Journal 2: 1408-1413.

Singh A, et al. (1963). Endemic fluorosis: Epidemiological, clinical and biochemical study of chronic fluoride intoxication in Punjab.Medicine 42: 229-246.

Singh A, et al. (1961). Skeletal fluorosis and its neurological complications. Lancet 1: 197-200.

Xu RQ, et al. (1997). Relations between environment and endemic fluorosis in Hohot region, Inner Mongolia. Fluoride 30: 26-28.