Pesticides chronic adverse effects

Prenatal and postnatal exposures to fenvalerate reduced prostate and seminal vesicle weights and plasma testosterone levels in male rats [55], A chronic study showed no adverse effects on reproductive tissues at a high dose level of 1,000 ppm [142]. In vivo and in vitro studies with rats and mice suggested that fenvalerate may affect male and female reproduction, possibly due to calcium transport alteration [143-146], One paper reported that fenvalerate affected human sperm count and sperm motility of male workers who were exposed to fenvalerate in a pesticide factory [147]. 

Federal agencies such as the FDA and EPA require a battery of toxicity tests in laboratory animals to determine an additive s or a pesticide s potential for causing adverse health effects, such as cancer, birth defects, and adverse effects on the nervous system or other organs. Tests are conducted for both short-term (acute) and long-term (chronic) toxicity. For chronic effects other than cancer, laboratory animals are exposed to different doses to determine the level at which no adverse effects occur. This level is divided by an uncertainty or safety factor (usually 100) to account for the uncertainty of extrapolating from laboratory animals to humans and for individual human differences in... 

Some khat leaves are grown with chemical pesticides. In 114 male khat users in two different mountainous areas of Yemen, users of khat that had been produced in fields in which chemical pesticides were used regularly had more acute gastrointestinal adverse effects (nausea and abdominal pain) and chronic body weakness and nasal problems (18). The authors suggested that organic chemical pesticides such as dimethoatecide can cause such adverse effects. 

In 1967, Frawley [7] analysed the results of over 200 chronic feeding studies in rodents and found that apart from a few exceptions (e.g. heavy metals, pesticides), there were no adverse effects observed at dietary levels below 100 ppm. Considering a safety factor of 1000 to cover any such exceptions, as well as considering the limited nature of his data base, he arrived at a figure of no-concem of 0.1 ppm (which translates to somewhere between 1 and 5 pg/kg body weight/day in consumers). 

Another major difference between the current approach and the previous approach for evaluating the adverse effects of pesticide exposure involves the way in which the toxicity data are interpreted. In the current system, the carcinogenicity data from the chronic rodent studies are extrapolated using mathematical models which provide a numerical estimate of the upper bound of the cancer risk, and these numbers (Q values) are then used for a variety of regulatory purposes. In essence, this approach substitutes mathematical guidelines for the scientific judgement that was the key element in the earlier approach. 

Endocrine and immunologic related adverse effects of pesticides are another example of an area where we need toxicologic testing methods that will detect both acute and chronic toxicity and provide a reliable basis for predicting human effects. Before we add new protocols to the current methodology, however, we need to evaluate the answers provided by our current methodology. 

An acute tolerance (MRL) assessment is routinely conducted by DPR to ensure that this level of residue will not result in adverse effects in consumers of treated commodities. It is the maximum amount of a pesticide residue dut is legally allowed on that commodity (14). By definition, the use of tolerance residue levels means that a point estimate, deterministic approach was used. DPR considers that acute, but not chronic, tolerance assessment is appropriate because it is highly improbable that an individual would consume a commodity with tolerance level residues on a chronic, annual basis. Similarly, it is considered by DPR to be inappropriate to use a percent crop-treated (%CT) adjustment on the tolerance assessment, whenever using a deterministic approach (Table VI). These tolerance assessments determined the MOS values at the 95 percentile of exposure. 

Humans can be exposed to POPs through diet, occupational exposures (for example, farmworkers may be exposed to POPs through pesticides), industrial accidents and the environment (including indoor exposure). Exposure to POPs, either acute or chronic, can be associated with a wide range of adverse health effects, including illness and death (L. Ritter et al., 1995). Laboratory animal studies and wildlife studies have associated POPs with endocrine disruption, reproductive and immune dysfunction, neurobehavioral disorders and cancer. More recently, some POPs have also been connected to reduced immunity in infants and children and a concomitant increase in infections. Other studies have linked POPS concentrations in humans with developmental abnormalities, neurobehavioral impairment and cancer and tumor induction or promotion.4... 

It is considered desirable to keep workplace exposure to pesticides as low as practical regardless of the current knowledge of their acute and chronic toxicity. All too often pesticides which were considered to be of negligible toxicity are later found to have a potential for causing adverse health effects following a sufficient period of exposure to an adequate dose. DBCP and nitrophen are good examples of this type of problem. We also gather and analyze detailed information on more than 2,000 illness reports per year from physicians who describe possible occupational exposures to specific pesticides. We also obtain or make detailed workplace measurements of the levels of pesticides to which workers may be exposed. 

---