TPS 633: Health effects of pesticides, Johan Friso Foyer, Floor 1, August 27, 2019, 3:00 PM - 4:30 PM Background: There is concern about residential exposure to pesticides and possible associated adverse health effects. Studies on this subject have been scarce with inconsistent results. We explored associations between residential proximity to specific crops, pesticide use and cause-specific mortality in The Netherlands, using individual level exposure and health data. Methods: From a national registration-based cohort (the Dutch Environmental Longitudinal Study (DUELS)), we selected inhabitants aged >30 living in less urbanized areas, at the same address for 9 years up to baseline (2005). This resulted in a cohort of >2.3 million individuals, followed for cause-specific mortality until 2012. We estimated the amount (kg) of fungicides, herbicides and insecticides used within buffers of 50, 100, 250 and 500 meters around each individual's residence as well as the area of specific crop groups (maize, grains, potatoes, beets, fruit, flower bulbs and other crops) cultivated within the same buffers for the period 1995-2003. The association between these exposure proxies and 28 mortality causes was investigated using Cox proportional hazards regression, adjusting for individual and area-level confounders. Results: After Bonferroni Correction we found lower mortality among individuals living close (<500m) to agricultural areas. We found no association between the use of pesticides and mortality. However, the presence of maize was associated with higher mortality from chronic lower respiratory diseases, showing a gradient with distance (HR [95% CI] per hectare of maize in the 50m buffer 1.242, [0.925, 1.667], 100m buffer 1.088, [1.000, 1.184], 250m buffer 1.014, [0.996, 1.032] and 500m buffer 1.006, [1.003, 1.010]). Results were further suggestive for an association between leukemia and the presence of cereals, beets and potatoes crops. Conclusions: Suggestive associations between crop area and cause-specific mortality emerged, while no associations were found with the amount of pesticides used. The reasons for this discrepancy are as yet unclear.
A quantitative risk assessment of health effects associated with particulate matter (PM), especially ambient PM10 levels, for the Netherlands has indicated premature mortality among approximately 1000 persons. Local information, including air pollution mix and health status of the population, has proven to be essential in such a risk assessment. One of the questions not answered yet is if smaller particles (PM2.5) are more toxic than PM10. According to the particle dosimetry models developed for the project, the local dose in the lungs of groups with a less than optimal health status may differ substantially when compared to healthy adults; this may partly explain differences in susceptibility. Modelling the Dutch and European emissions of PM and precursor gasses with an air pollution dispersion model has indicated that part (nearly half) of the Dutch yearly PM10 averages are still unaccounted for. A monitoring programme has been started to determine the composition of the missing PM10 and its sources. An extensive programme of experimental inhalation toxicology using a mobile particle concentrator has also been developed to conform to epidemiological associations and more specifically to the discovery of causative fractions (and their sources). In vitro tests with lung tissue taken from a variety of individuals demonstrated great variability between these individuals in their susceptibility to collected ambient PM of different-sized fractions at the different locations. A scientific workshop, envisaged for mid-2001, will allow a wider application of the results, with answers to the questions of the Ministry of Housing, Spatial Planning and Environment possibly expected by the beginning of 2002.
Dit onderzoek beoogde een studie naar de mogelijke ontwikkeling van tolerantie en uiteindelijke irreversibele effecten in long door schade na herhaalde blootstelling aan NO2. Hiertoe werden ratten blootgesteld aan 9 mg NO2/m3, of aan 3 mg NO2/m3 als achtergrond concentratie, aangevuld met 2 perioden van een uur per dag van 9 mg NO2/m3 gedurende vijf dagen. Na een expositie periode van een week ademden de dieren gedurende de tweede week schone lucht. Dit schema van twee weken werd zesmaal herhaald. Licht- en elektronenmicroscopisch onderzoek op de long werden uitgevoerd op de dagen 7, 14, 35, 77, 85 en 99. Resultaten van deze studie laten zien, dat voor de groep die continue werd blootgesteld aan 9 mg NO2/m3, de morfologische effecten identiek waren na elke expositie periode, behalve dat na de derde (dag 35) en zesde expositie week (dag 77) de hypertrofie van het bronchiolair epithelium minder was in vergelijking met de lesie na de eerste expositie week. Het lijkt dat tenminste voor deze morfologische entiteit er een indicatie voor tolerantie bestaat. Een week na het beeindigen van elke expositie periode waren de longen van de blootgestelde ratten volledig hersteld, en lieten geen verschil met de controle dieren zien, uitgezonderd de aanwezigheid van gedesorienteerde basaallichaampjes in trilhaarcellen. Ratten die blootgesteld werden aan 3 mg NO2/m3 als achtergrond concentratie, aangevuld met twee perioden van een uur per dag van 9 mg NO2/m3, vertoonden geen verschillen met de controle dieren.
AbstractThe evidence is inconclusive as to whether age and gender are important determinants of ozone toxicity We carried out an experiment to investigate the possible age- and gender-related differences in pulmonary toxicity following both acute and repeated exposure to ozone. Male and female rats of various ages (1, 3, 9, and 18 mo) were exposed to 0.8 mg O3/m3 for 1 day (12 h) or for 7 days (12 h/day) during the dark period. Bronchoalveolar lavage (BAL) and biochemical, histopathological, and immunological techniques were used to determine the permeability, antioxidant capacity, tissue morphology, and extent of inflammation in the lungs. Morphological as well as morphometric results showed age-related differences in the extent of pulmonary lesions after 1 and 7 days of ozone exposure; from the age of 3 mo animals became less susceptible to ozone. Pulmonary antioxidant enzyme capacity in control rats appeared to exhibit an age-related decline starting at 3 mo. However, exposure to ozone resulted in an increase in enzyme activities in rats aged 9 and 18 mo. There was no significant overall age-related effect of ozone. However, a different pattern existed between both sexes in their age-related reaction to ozone exposure. The percentage increase of protein and albumin concentrations in BAL increased after acute ozone exposure, peaking at the age of 1 mo. The lesser increase at the age of 9 and 18 mo suggests a decreasing sensitivity in older rats. The gradual decrease of the net percentage of polymorphonuclear leukocytes (PMNs) in BAL after ozone exposure in male rats with age corroborates this suggestion. Ozone exposure decreased the clearance of Listeria bacteria in lungs. There was no significant difference between the various age groups in the resistance to Listeria infection after ozone exposure. It can therefore be concluded that specific toxicity indices including lung tissue damage, increased permeability, and inflammation point to a more pronounced responsiveness of younger animals to ozone. No gender-related differences in the response to ozone were observed for any of the parameters examined. These data support the view that age is a significant predictor of the pulmonary response to ozone, with younger subjects being more sensitive.
The aim of this study is to assess whether medication use for obstructive airway diseases is associated with environmental exposure to livestock farms. Previous studies in the Netherlands at a regional level suggested that asthma and chronic obstructive pulmonary disease (COPD) are less prevalent among persons living near livestock farms.A nationwide population-based cross-sectional study was conducted among 7,735,491 persons, with data on the dispensing of drugs for obstructive airway diseases in the Netherlands in 2016. Exposure was based on distances between home addresses and farms and on modelled atmospheric particulate matter (PM10) concentrations from livestock farms. Data were analysed for different regions by logistic regression analyses and adjusted for several individual-level variables, as well as modelled PM10 concentration of non-farm-related air pollution. Results for individual regions were subsequently pooled in meta-analyses.The probability of medication for asthma or COPD being dispensed to adults and children was lower with decreasing distance of their homes to livestock farms, particularly cattle and poultry farms. Increased concentrations of PM10 from cattle were associated with less dispensing of medications for asthma or COPD, as well (meta-analysis OR for 10th-90th percentile increase in concentration of PM10 from cattle farms, 95%CI: 0.92, 0.86-0.97 for adults). However, increased concentrations of PM10 from non-farm sources were positively associated (meta-analysis OR for 10th-90th percentile increase in PM10-concentration, 95%CI: 1.29, 1.09-1.52 for adults).The results show that the probability of dispensing medication for asthma or COPD is inversely associated with proximity to livestock farms and modelled exposure to livestock-related PM10 in multiple regions within the Netherlands. This finding implies a notable prevented risk: under the assumption of absence of livestock farms in the Netherlands, an estimated 2%-5% more persons (an increase in tens of thousands) in rural areas would receive asthma or COPD medication.
Information on the relationship between levels of particulate matter (PM) smaller than 2.5 μm and mortality rates in Europe is relatively sparse because of limited availability of PM2.5 measurement data. Even less information is available on the health effects attributable to PM2.5-10, especially for North-West Europe.To investigate the relationship between various PM size fractions and daily mortality rates.Daily concentrations of PM from the Dutch National Ambient Air Quality Monitoring Network as well as all cause and cause-specific mortality rates in The Netherlands were obtained for the period 2008-2009. Poisson regression analysis using generalized additive models was used, with adjustment for potential confounding including long-term and seasonal trends, influenza incidence, meteorological variables, day of the week, and holidays. Different measures of PM (PM2.5, PM10 and PM2.5-10) were analysed.PM10 and PM2.5 levels were statistically significantly (p<0.05) associated with all cause and cause-specific deaths. For example, a 10 μg/m(3) increase in previous day PM was associated with 0.8% (95% CI 0.3-1.2) excess risk in all cause mortality for PM2.5 and a 0.6% (CI 0.2-1.0) excess risk for PM10. No appreciable associations were observed for PM2.5-10. Effects of PM10, and PM2.5 were insensitive to adjustment for PM2.5-10, and vice-versa. PM10 and PM2.5 were too highly correlated to disentangle their independent effects.PM10 and PM2.5 both were significantly associated with all cause and cause-specific mortality. We were unable to demonstrate significant effects for PM2.5-10, possibly due to the lower temporal variability and the higher exposure misclassification in PM2.5-10 compared to PM10 or PM2.5. The lack of effects of PM2.5-10 in our study should therefore not be interpreted as an indication that PM2.5-10 can be considered harmless.