Endosulfan’s Effects: Saiyed’s Response

I would like to respond to the comments of both Abraham and Indulkar about the origin and results of our study (Saiyed et al. 2003).

On the basis of media reports of unusual illnesses in Padre village, we were asked by the National Human Rights Commission to investigate these illnesses and determine if they were linked to endosulfan exposure. These reported illnesses consisted of birth defects, growth- and development-related problems in children, neurologic disorders, epilepsy, allergic disorders, cancers, and high rates of suicide. On the basis of our site visit, study of the topography of the area, the report of the Regional Remote Sensing Service Centre (Nageswara Rao PP, personal communication), and information from the Plantation Corporation of Kerala (PCK), we determined that we had a unique opportunity to study various health effects of long-term exposure to endosulfan on human health.

Our study (Saiyed et al. 2003) had two components: a) an investigation of growth-and development-related parameters, such as physical growth (height and weight), skin-fold thickness, IQ, study of behavioral problems and scholastic performance, sexual maturity rating (SMR), and an estimation of sex hormones, in schoolchildren exposed to the aerial spray of endosulfan; and b) an investigation of diseases, such as neurologic and psychiatric disorders, infertility, and allergic disorders, in the adult population, which was carried out through secondary data collection from parents of the children.

In our report submitted to the National Human Rights Commission, [National Institute of Occupational Health (NIOH) 2002], we reported a higher prevalence of birth defects in both male and female children, lower mean SMR and serum testosterone levels in male children of similar age, a higher prevalence of scholastic backwardness, and neurobehavioral problems in children who had been exposed to endosulfan through aerial treatment of fields (NIOH 2002). We suggested a possible link between endosulfan exposure and these problems, which has been reported in a number of published animal experimental studies, for example, endosulfan-related birth defects (Food Machinery and Chemical Corporation 1980; García-Rodríguez et al. 1996; Gupta et al. 1978]; scholastic development (Lakshmana and Raju 1994; Paul et al. 1994); and reproductive effects in males (Dalsenter et al. 1999; Sinha et al. 1997, 2001). We submitted our report to the Registration Committee at their request. The eight-member expert committee, which included two major stakeholders of endosulfan in the country, was set up by the Registration Committee to examine our report along with the report of the Kerala Agriculture University (KAU) and the Fredrick Institute of Plant Protection and Toxicology (FIPPAT). The committee raised issues, many of which are also mentioned in the letters from Abraham and Indulkar, and remarked that “the findings of the NIOH study are not in conformity with the known and accepted properties, chemistry and toxicology of endosulfan” (Dubey 2003). The committee concluded that the study did not establish a link between endosulfan exposure and the health problems in Padre village. The decision of the committee was not unanimous.

One of the important components of any scientific investigation is dissemination of information to other scientists through publication of the results in a suitable journal; therefore, we submitted a manuscript covering part of the study to EHP. The opinion of the expert committee and their deliberations in no way affected our right of scientific communication. Our study was scientifically planned, designed, and carried out by a team of experts, which included epidemiologists, physicians, pediatricians, medical toxicologists, statisticians, analytical chemists, and biochemists, who have years of experience in conducting such studies and have many publications to their credit. Our article (Saiyed et al. 2003) was based on a portion of the results of the study in children. Some of the other parameters related to growth and development will be communicated at a later date.

Both Abraham and Indulkar comment that several pesticides were used in the area, so endosulfan cannot be blamed for the reported health problems. Based on the topographic study of the area, we were concerned about what was sprayed on the cashew plantation, which covered a very large area on the hills; we believed that compounds sprayed on the plantation would run off into streams used by residents of the village downhill from the plantation. We asked the PCK, the owners of the cashew plantation, to give us information on all pesticides that were sprayed in the study area. On 20 August 2001, PCK informed us that since 1980 they had aerially sprayed endosulfan (0.1% of 35% emulsifiable concentrate) twice a year almost every year. They did not mention the use of any other pesticides. In their letters, Abraham and Indulkar mention the use of other pesticides in the area; this probably refers to the valley where there are small farms that are owned by the local families. The major crop in this valley and in the control area is areca nut, for which Bordeaux mixture (copper sulfate and lime) is used. The small family farms in the valley and in the control village had a similar crop pattern; therefore, we can assume localized ground use of pesticides. This type of localized pesticide use is unlikely to cause significant widespread exposure. Our conclusions (Saiyed et al. 2003) were based on the comparison of the control and study areas on the basis of aerial exposure; therefore, the use of other pesticides, if similar in both the study and control areas, would not affect our conclusions. The issue of finding endosulfan in serum samples of the control population was adequately addressed in the “Discussion” of our article (Saiyed et al. 2003).

In their letters, Abraham and Indulkar comment that downward movement of the pesticides could start only at the onset of monsoons 5–6 months after exposure, by which time no endosulfan would remain because it biodegrades rapidly. The NIOH and three other agencies carried out endosulfan analyses at varying times (January 2001–August 2001) and reported significant amounts of endosulfan in various environmental media. First, the Centre for Science and Environment, New Delhi (a nongovernment organization), analyzed biological and environmental samples for endosulfan residues in January 2001, 1 month after the last aerial spray of endosulfan carried out on 26 December 2000. The results showed that the concentration of endosulfan in three water samples was 7–51 times higher than the maximum residue limit (MRL) (Joshi 2001). Very high levels of endosulfan were reported in samples of human blood, human milk, vegetables, spices, cow’s milk, animal tissues, cashews, cashew leaves, and soil. In one of the soil samples, the concentration of endosulfan was 391 times higher than the MRL.

Second, the KAU, Thrissur District (Kerala), India, studied endosulfan levels in soil (n = 4), plants (n = 5), water (n = 5), and sediment (n = 1) in the pond in the valley on 19 February 2001 using an HPLC–spectrophotometric detector technique. They reported endosulfan in soil (3,815 ppb on PCK plantation), 55 ppb in the mid-hills, and 315 ppb in the sediment in the pond (Mathew S, personal communication). They also reported 507–858 ppb endosulfan in cashew leaves. Their report clearly demonstrated downward movement of endosulfan from hills to the pond water (Figure 1). (Mathew S, personal communication).

Figure 1. Altitude-wise distribution of endosulfan. ND, not detected. Reproduced with permission from Samuel Mathew, Department of Chemistry, Kerala Agriculture University.

Third, FIPPAT, Padappai, India, carried out sampling between March and May 2001 in cashew leaves (n = 28), human blood (n = 112), water (n = 30), and soil (FIPPAT 2001). The authors reported up to 3,430 ppb endosulfan in cashew leaves, 1–11 ppb in soil, and no endosulfan in blood or water samples. On examination of the report (FIPPAT 2001), we noted large peaks of alpha- and beta-endosulfan in some chromatographs of soil, leaf, and blood samples that they had not mentioned. We reported this discrepancy to the expert committee and requested action.

The results of the studies by the Centre for Science and Environment in January 2001 (Joshi 2001), the KAU in February 2001 (Mathew S, personal communication), and FIPPAT (2001) in March–May 2001 clearly indicate significant translocation of endosulfan from the hills to the valley and its persistent nature.

Abraham and Indulkar both noted a discrepancy in our article (Saiyed et al. 2003) between endosulfan levels in serum and water. They both assume that the endosulfan exposure occurred only through water, which is not correct. Endosulfan adhers to the soil particles; runoff water then carries the endosulfan attached to soil particles from leaf surfaces and the ground during the first few rainfalls. Also, winter rains are common in this area of India. This view is largely supported by the KAU study (Mathew S, personal communication), which showed high levels of endosulfan (315 ppb) in pond sediment in the study village. Endosulfan attached to soil particles can enter the body through the dermal route, more so in a hot and humid climate (excessive sweating), and through ingestion, particularly in children, who commonly have hand-to-mouth behavior. Endosulfan attached to the soil particles can also be translocated through other environmental media.

Indulkar raised several points about the results of our article (Saiyed et al. 2003). He incorrectly stated that we found poor correlation of SMR and hormone levels with age; our correlations are shown in Tables 2 and 3 of our article (Saiyed et al. 2003). He also complained that we had not compared the ranges of SMR and hormone levels in our study groups to normal ranges, but we did not consider it necessary because we were comparing the groups with each other. Also, Indulkar’s points about the wide variability of hormone levels and small sample size were discussed and clarified in our article.

Both Abraham and Indulkar stated that endosulfan cannot travel a distance of 3–4 km and that it biodegrades quickly. The long half-life of endosulfan in soil is well known and was mentioned in our “Discussion” (Saiyed et al. 2003). The U.S. Environmental Protection Agency (EPA 2002) reported that

Endosulfan is a volatile and persistent cyclodiene pesticide that can migrate over a long distance through various environmental media such as air, water and sediment. Once endosulfan is applied to crops, it can either persist in soil as a sorbed phase or be removed through several physical, chemical and biological processes. Recent studies suggest that secondary emissions of residual endosulfan continue to recycle in the global system while they slowly migrated and are rede-posited via wet deposition in the Northern Hemisphere. The occurrence of endosulfan in remote regions like the Great Lakes, the Arctic and the mountainous areas is well documented. Endosulfan can also enter the air as adsorbed phase onto suspended particulate matter, but this process does not appear to be a major contributor to long range transport like volatilization.

The information provided above further supports the comment made by Jim Burkhart, EHP Science Editor, that

Decades of spraying this pesticide, and only this pesticide, on the village provided a unique opportunity to analyze its impact. Although the sample size was somewhat limited, the results are quite compelling.

We stand by the conclusions in our article (Saiyed et al. 2003).