Allergens in indoor air: environmental assessment and health effects.

It has been suggested that the increase in morbidity and mortality for asthma and allergies, may also be due to an increase in exposure to allergens in the modern indoor environment. Indoor allergen exposure is recognised as the most important risk factor for asthma in children. House dust mites, pets, insects, plants, moulds and chemical agents in the indoor environment are important causes of allergic diseases. House dust mites and their debris and excrements that contain the allergens are normally found in the home in beds, mattresses, pillows, carpets and furniture stuffing, but they have also been found in office environments. Domestic animals such as cats, dogs, birds and rodents may cause allergic asthma and rhinoconjunctivitis. The exposure usually occurs in homes, but also in schools and kindergartens where domestic animals are kept as pets or for education; moreover, cat and dog owners can bring allergens to public areas in their clothes. Allergy to natural rubber latex has become an important occupational health concern in recent years, particularly among healthcare workers; when powdered gloves are worn or changed, latex particles get into the air and workers are exposed to latex aerosolised antigens. To assess the environmental risk to allergen exposure or to verify if there is a causal relationship between the immunologic findings in a patient and his/her environmental exposure, sampling from the suspected environment may be necessary.

Assessment through environmental and biological measurements of total daily exposure to volatile organic compounds of office workers in Milan, Italy.

Personal exposure to total volatile organic compounds (TVOCs), benzene and toluene of 100 Milan office workers was assessed through personal air monitoring at home, in the office, and during commuting. Biological monitoring was performed by measuring blood benzene and toluene concentrations together with urinary trans-trans-muconic acid (t,t-MA) and cotinine at the end of the monitoring period. The geometric means of the total 24-h personal exposure were 514 micrograms/m3 for TVOCs, 21.2 micrograms/m3 for benzene and 35.2 micrograms/m3 for toluene. Daily exposure to the volatile organic compounds was almost totally determined by indoor exposure at home and in the office, with a minor contribution in the transport means. An important factor determining exposure to benzene was found to be tobacco smoke, both for active smokers and for non-smokers exposed to environmental tobacco smoke (ETS). All the mean levels of the biological indicators were significantly higher in active smokers than in non-smoking subjects non-exposed to ETS; urine cotinine and t,t-MA levels were also significantly higher in non-smokers exposed to ETS than in non-smokers non-exposed to ETS.

Seasonal effect on airborne pyrene, urinary 1-hydroxypyrene, and benzo(a)pyrene diol epoxide-hemoglobin adducts in the general population.

Exposure to airborne polycyclic aromatic hydrocarbons (PAHs) in 65 employees (40 sampled both in summer and winter, 15 sampled in summer only, and 10 sampled in winter only) with no occupational exposure to PAHs was assessed by measuring: personal exposure to pyrene, urinary excretion of 1-hydroxypyrene (1-OHP), and benzo(a)pyrene diol epoxide adducts to hemoglobin (BPDE-Hb). Overall, office employees were exposed to significantly higher levels of pyrene in winter (4.54 +/- 2.35 ng/m3, mean +/- SD) than in summer (1.67 +/- 1.92 ng/m3, mean +/- SD; P < 0.001), but no such seasonal variability was observed in 1-OHP excretion. Tobacco smoking was the major determinant of 1-OHP excretion. BPDE-Hb adducts were measured by gas chromatography-mass spectrometry as benzo(a)pyrene tetrols (BPT) released from adducted hemoglobin. In the 65 employees analyzed, mean BPT levels +/- SD were higher in winter (0.14 +/- 0.38 fmol/mg Hb) than summer (0.031 +/- 0.022 fmol/mg Hb). This difference was not statistically significant, probably because of the small proportion of subjects with detectable adducts (11% in summer and 16% in winter). BPDE-Hb adducts were not significantly associated with sex, age, diet, smoking habits, or with pyrene levels and 1-OHP excretion. This is the first report providing reference BPDE-Hb adduct values for the general population not occupationally exposed to environmental PAHs and shows a tendency to seasonal variability, with higher BPT levels in winter when environmental PAHs are also high.

Immunomodulatory effects of occupational exposure to mancozeb.

The effects of occupational exposure to ethylene-bis-dithiocarbamate of manganese and zinc on the immune system were evaluated in a group of mancozeb-exposed manufacturers and controls. The immune system tests revealed the following: (a) lymphocyte proliferative responses triggered by different activators and mitogen-induced IL-2 production were higher in exposed subjects than in controls; (b) production of monocyte/macrophage-derived IL-1 and polyclonal IgG and IgM, by beta-lymphocytes, did not differ between exposed subjects and controls; (c) percentages and absolute numbers of total T-cells, T-helper cells, T-suppressor/cytotoxic cells, activated T-cells, total beta-cells, and natural killer cells were similar in exposed subjects and controls; (d) serum immunoglobulin classes and complement fractions were within the range of normality; and (e) rheumatoid factor and non-organ-specific serum autoantibodies were absent in exposed and control subjects. An increase in T-cell functional response was found in the exposed group, suggesting a slight immunomodulator effect of mancozeb in conditions of low-level, prolonged occupational exposure.

Toxicological and immune findings in workers exposed to pentachlorophenol (PCP).

Pentachlorophenol (PCP) is a pesticide used worldwide in industrial and domestic applications. Data available on the effects of technical-grade PCP on the immune system are insufficient and equivocal; some data indicate inhibitory effects, whereas others suggest stimulating effects. This study was performed to evaluate toxicological and immune findings in 32 subjects who had prolonged exposure to PCP in a wood factory and in 37 controls. PCP concentrations were determined in plasma and urine of all subjects. Lymphocyte subsets of CD3-, CD4-, and CD8-positive cells were evaluated, and the proliferative response of peripheral blood mononuclear cells (PBM) to mitogens was assessed. The results suggested the absence of major laboratory and clinical signs of PCP-dependent immune deficiency. A weak effect of long-term exposure to PCP on the functional immune response could not be ruled out because of the finding of a decreased response to 5% PHA in the high-exposure group. A weak effect against hepatocyte membrane was evidenced by the finding of raised serum concentration of glycocholic, taurodeoxycholic, and glycochenodeoxycholic acids in subjects directly exposed to PCP for more than 10 y.

The fast acetylator phenotype in diabetes mellitus: abnormal prevalence and association with the ABO blood groups.

The acetylator phenotype and ABO blood groups were evaluated in 55 normal subjects and in 156 diabetic patients [61 with Type 1 (insulin-dependent) diabetes and 95 with Type 2 (non-insulin-dependent) diabetes]. The prevalence of fast acetylators was significantly higher in the Type 1 diabetic patients (53%) than in the control subjects (29%). In the Type 2 diabetic patients the prevalence was 39%, and thus not significantly different from the control or Type 1 diabetic groups. In the Type 2 diabetic patients, but not in the control or in the Type 1 diabetic subjects, an association between the fast acetylator phenotype and the B blood group was found.