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There is increasing evidence that inflammatory mechanisms other than eosinophilic inflammation may be involved in producing the final common pathway of enhanced bronchial reactivity and reversible airflow obstruction that characterises [...]

Objectives: To compare respiratory symptoms and upper airway inflammation in domestic waste collectors and controls, and to find the association between measures of upper airway inflammation on the one hand [...]

The evidence as to whether exposure to environmental airborne endotoxin plays a protective or an inducing role in the development of asthma is reviewed. Studies of endotoxin and atopy, endotoxin [...]

ObjectivesTo assess associations between occupational exposures to pesticides and other chemicals and motor neuron disease (MND).MethodsA population-based case–control study that included 319 MND cases (64% male/36% female) recruited through the New Zealand MND Association complemented with hospital discharge data, and 604 controls identified from the Electoral Roll. For each job held, a questionnaire collected information on 11 exposure categories (dust, fibres, tobacco smoke, fumes, gas, fumigants, oils/solvents, acids/alkalis, pesticides, other chemicals and animals/animal products). ORs were estimated using logistic regression adjusting for age, sex, ethnicity, socioeconomic status, education, smoking, alcohol consumption, physical activities, head/spine injury and other occupational exposures.ResultsTwo exposure categories were associated with increased MND risks: pesticides (OR 1.70, 95% CI 1.17 to 2.48) and fumigants (OR 3.98, 95% CI 1.81 to 8.76), with risks increasing with longer exposure duration (p<0.01). Associations were also observed for: methyl bromide (OR 5.28, 95% CI 1.63 to 17.15), organochlorine insecticides (OR 3.28, 95% CI 1.18 to 9.07), organophosphate insecticides (OR 3.11, 95% CI 1.40 to 6.94), pyrethroid insecticides (OR 6.38, 95% CI 1.13 to 35.96), inorganic (copper) fungicides (OR 4.66, 95% CI 1.53 to 14.19), petrol/diesel fuel (OR 2.24, 95% CI 1.27 to 3.93) and unspecified solvents (OR 1.91, 95% CI 1.22 to 2.99). In women, exposure to textile fibres (OR 2.49, 95% CI 1.13 to 5.50), disinfectants (OR 9.66, 95% CI 1.29 to 72.44) and cleaning products (OR 3.53, 95% CI 1.64 to 7.59) were also associated with MND; this was not observed in men (OR 0.80, 95% CI 0.44 to 1.48; OR 0.72, 95% CI 0.29 to 1.84; OR 0.57, 95% CI 0.21 to 1.56, respectively).ConclusionsThis study adds to the evidence that pesticides, especially insecticides, fungicides, and fumigants, are risk factors for MND.

Abstract Objectives--Exposure to high levels of non-infectious microbial agents is recognised as a cause of respiratory disease in working populations, but except for endotoxins, little is known about exposure-response relations. [...]

In recent decades a number of authors have argued that allergen exposure is the major primary cause of asthma, and that the global increases in asthma prevalence are due to increases in exposure to aeroallergens. We have assessed the epidemiological evidence in support of this hypothesis. No longitudinal studies were identified in which allergen exposure during infancy in a random population sample has been related to asthma risk after the age of six years. Two studies have been conducted in selected populations chosen on the basis of a family history of asthma or allergy; one study found a non-statistically significant association whereas the other study found no association. Many of the identified prevalence studies in children showed negative associations between allergen exposure and current asthma, and the weighted averages of the population attributable risks in children were 4% for Der p 1, 11% for Fel d 1, -4% for Bla g 2, and 6% for Can f 1. There was little change in these estimates in studies in which children whose parents had adopted allergen avoidance measures were excluded. Furthermore, evidence from population studies is equivocal and provides little consistent evidence that allergen exposure is associated with the prevalence of asthma at the population level. Population-based cohort studies are clearly required, but currently available evidence does not indicate that allergen exposure is a major risk factor for the primary causation of asthma in children.

Early life exposures to microbial agents such as bacterial endotoxin have been suggested to inhibit the development of atopy and asthma. In this study we assessed the relation between living room floor levels of bacterial endotoxin, fungal ß(1,3)-glucan and fungal extracellular polysaccharides (EPS-Pen/Asp) and the development of atopic sensitisation and asthma in 810 infants born from allergic parents. Exposure to microbial agents was determined at 3 months, serum IgE at 12 and 24 months, and asthma symptoms & diagnosis at 12, 24, and 48 months. Low, medium and high exposure groups were defined based on tertiles of the exposure distributions. Analyses were adjusted for gender, pets, ETS, siblings, parental education, and mite allergen levels. Microbial exposure was inversely associated with atopic sensitization at 24 months in a dose dependent manner with ORs ranging from 0.3–0.5 for the highest exposure groups (statistically significant only for EPS-Pen/Asp). A similar but weaker dose response was observed for atopy at 12 months. A doctor's diagnosis of asthma at 48 months was also less common in highly exposed children with ORs ranging from 0.3–0.5, statistically significant (p < 0.01) for endotoxin and EPS. A protective effect in the medium exposure group was also observed but the effect was less pronounced suggesting a dose-response effect. These protective effects on doctor's diagnosed asthma were shown consistently across the three time points, but were statistically significant only at 24 and 48 months. Interestingly, the protective effects of microbial exposure were observed both in atopic and non-atopic asthmatics. Asthma symptoms (wheeze and night cough) in the last 12 months (at age 4) were slightly less prevalent in the high exposure groups (NS). No associations were found for eczema. Endotoxin, EPS-Pen/Asp, and glucan concentrations were highly correlated limiting the potential to study them separately. In conclusion, although our findings need confirmation at older ages, they provide, for the first time, evidence from a prospective cohort study that non-infectious microbial exposure at a very young age may protect from developing atopy and asthma.