Parkinson’s disease (PD) is an idiopathic disease of the nervous system characterized by progressive tremor, bradykinesia, rigidity, and postural instability. It has been postulated that exogenous toxicants, including pesticides, might be involved in the etiology of PD. In this article we present a comprehensive review of the published epidemiologic and toxicologic literature and critically evaluate whether a relationship exists between pesticide exposure and PD. From the epidemiologic literature, there does appear to be a relatively consistent relationship between pesticide exposure and PD. This relationship appears strongest for exposure to herbicides and insecticides, and after long durations of exposure. Toxicologic data suggest that paraquat and rotenone may have neurotoxic actions that potentially play a role in the development of PD, with limited data for other pesticides. However, both the epidemiology and toxicology studies were limited by methodologic weaknesses. Particular issues of current and future interest include multiple exposures (both pesticides and other exogenous toxicants), developmental exposures, and gene–environment interactions. At present, the weight of evidence is sufficient to conclude that a generic association between pesticide exposure and PD exists but is insufficient for concluding that this is a causal relationship or that such a relationship exists for any particular pesticide compound or combined pesticide and other exogenous toxicant exposure.

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Objectives-Benzene has long been recognised as a carcinogen and recent concern has centred on the eVects of continuous exposure to low concentrations of benzene both occupationally and environmentally. This paper presents an overview of the current knowledge about human exposure to benzene in the United Kingdom population based on recently published data, summarises the known human health eVects, and uses this information to provide a risk evaluation for sections of the general United Kingdom population. Method-Given the minor contribution that non-inhalation sources make to the overall daily intake of benzene to humans, only exposure from inhalation has been considered when estimating the daily exposure of the general population to benzene. Exposure of adults, children, and infants to benzene has been estimated for diVerent exposure scenarios with timeactivity patterns and inhalation and absorption rates in conjunction with measured benzene concentrations for a range of relevant microenvironments. Exposures during refuelling and driving, as well as the contribution of active and passive tobacco smoke, have been considered as part of the characterisation of risk of the general population. Results-Infants (<1 years old), the average child (11 years old), and nonoccupationally exposed adults, receive average daily doses in the range of 15-26, 29-50, and 75-522 µg of benzene, respectively, which correspond to average ranges to benzene in air of 3.40-5.76 µg/m 3 , 3.37-5.67 µg/m 3 , and 3.7-41 µg/m 3 for infants, children, and adults, respectively. Infants and children exposed to environmental tobacco smoke have concentrations of exposure to benzene comparable with those of an adult passive smoker. This is a significant source of exposure as a 1995 United Kingdom survey has shown that 47% of children aged 2-15 years live in households where at least one person smokes. The consequence of exposure to benzene in infants is more significant than for children or adults owing to their lower body weight, resulting in a higher daily intake for infants compared with children or non-smoking adults. A worst case scenario for exposure to benzene in the general population is that of an urban smoker who works adjacent to a busy road for 8 hours/day-for example, a maintenance worker-who can receive a mean daily exposure of about 820 µg (equal to an estimated exposure of 41 µg/m 3 ). The major health risk associated with low concentrations of exposure to benzene has been shown to be leukaemia, in particular acute non-lymphocytic leukaemia. The lowest concentration of exposure at which an increased incidence of acute nonlymphocytic leukaemia among occupationally exposed workers has been reliably detected, has been estimated to be in the range of 32-80 mg/m 3 . Although some studies have suggested that eVects may occur at lower concentrations, clear estimates of risk have not been determined, partly because of the inadequacy of exposure data and the few cases. Conclusions-Overall the evidence from human studies suggests that ...

ObjectiveClimate change is likely to affect the nature of pathogens and chemicals in the environment and their fate and transport. Future risks of pathogens and chemicals could therefore be very different from those of today. In this review, we assess the implications of climate change for changes in human exposures to pathogens and chemicals in agricultural systems in the United Kingdom and discuss the subsequent effects on health impacts.Data sourcesIn this review, we used expert input and considered literature on climate change; health effects resulting from exposure to pathogens and chemicals arising from agriculture; inputs of chemicals and pathogens to agricultural systems; and human exposure pathways for pathogens and chemicals in agricultural systems.Data synthesisWe established the current evidence base for health effects of chemicals and pathogens in the agricultural environment; determined the potential implications of climate change on chemical and pathogen inputs in agricultural systems; and explored the effects of climate change on environmental transport and fate of different contaminant types. We combined these data to assess the implications of climate change in terms of indirect human exposure to pathogens and chemicals in agricultural systems. We then developed recommendations on future research and policy changes to manage any adverse increases in risks.ConclusionsOverall, climate change is likely to increase human exposures to agricultural contaminants. The magnitude of the increases will be highly dependent on the contaminant type. Risks from many pathogens and particulate and particle-associated contaminants could increase significantly. These increases in exposure can, however, be managed for the most part through targeted research and policy changes.

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