Many pesticides are considered to be persistent chemicals, which means they are resistant to degradation and have become widespread contaminants throughout the environment. Because of their lipophilic qualities, they are known to accumulate in the fatty tissue of animals, including humans. The ability of these persistent compounds to bioaccumulate allows for transfer of the contaminant to the fetus through the placenta and to infants through breast milk (Tryphonas 1998; Vial et al. 1996). However, a recent study by Karmaus and colleagues indicates that contaminant pesticide in breast milk may negate the protective effect of breast milk on atopic manifestations (Karmaus et al. 2003).
Exposure to pesticides has been reported to cause a number of immunotoxic effects: hypersensitivity, autoimmunity, modulation of immune function, and clinical immunosuppression. Several authors have recently reviewed pesticide immunotox-icity (Banerjee 1999; Colosio et al. 1999; Thomas 1995; Vial et al. 1996; Voccia et al. 1999). The majority of studies investigating the effects of pesticides on the human immune system involve relatively high-level occupational exposures. Few studies have investigated pesticide immunotoxicity in the general population at relevant, environmental exposure levels (Thomas 1995).
More specifically, there has been very little research on the influence of exposure to persistent pesticides and either the development or exacerbation of the allergic asthma response or other atopic manifestation (Ernst 2002). A few epidemiological studies have found significant associations between asthma and other respiratory health problems and occupational (i.e., high-level) exposure to certain pesticides and various allergens in rural and agricultural settings (reviewed in: Vial et al. 1996; National Academy of Sciences 2000). The relevance of these studies to potential links between asthma exacerbation and lower-level pesticide exposures is not known. The mechanism of the reported asthma-like response in these studies is poorly understood, and there has only been one study indicating an immunologically mediated response directed against a pesticide molecule (see 'Polycyclic Halogenated Hydrocarbons" section below).
Several studies in animals have shown that prenatal and neonatal exposure to organochlorine pesticides, such as chlordane, toxaphene, and hexachlorobenzene, does have significant effects on the developing immune system. These effects on the immune system are persistent and occur at dose levels that do not elicit effects in adult animals. However, the endpoints assessed in the studies are largely indicative of immunosuppressive effects rather than atopic or allergic responses (Thomas, 1995; Voccia et al. 1999). Whether the immunosuppression reported in these studies could be TH1-specific and thereby favor TH2-mediated diseases such as asthma will have to be borne out in further, more narrowly defined studies.
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.