Polybrominated diphenyl ethers and organochloride pesticides in the organic matter of air suspended particles in Mexico valley: A diagnostic to evaluate public policies.

The presence of organochlorine pesticides (OCPs) and polybrominated diphenyl ethers (PBDEs) was analysed in air particulate matter ≤ 2.5 µm (PM2.5) and ≤10 µm (PM10) collected in the Metropolitan Zone of Mexico Valley (MZMV), during 2013 and 2014, respectively. Spatial and seasonal distributions of PM and their organic content named solvent extracted organic matter (SEOM) were determined. PM mass concentration and SEOM/PM ratios were compared with previous studies in 2006 in Mexico City. PM2.5 concentration was like found in 2006, however, PM10 decreased ∼43%. The SEOM/PM10 ratio was kept constant, suggesting a decrease in SEOM as well as PM10 emitted from natural sources, probably as a result of changes in the land use due to urban growth. A decrease ∼50% SEOM/PM2.5 ratio was observed in the same period, linked to adequate strategies and public policies applied by the local and federal governments to control the organic matter emitted from anthropogenic sources. Seven out of sixteen OCPs and five out of six PBDEs were found. The most common POPs were endosulfan I, endosulfan II, endosulfan sulfate, BDE-47 and BDE-99, present on >90% of the sampling days. OCPs in PM2.5 and PBDEs in PM10 showed seasonal variability. Higher PBDEs concentration in both particle sizes were observed at east and southeast of the MZMV, where one of the biggest landfills and wastewater treatment plants are located. OCPs in PM10 were mainly emitted from agricultural areas located to the southwest, southeast and east of the MZMV. OCPs in PM2.5 showed a regional contribution from the north and introduced into the valley. OCP degradation products were dominant over native OCPs, indicating no fresh OCP use. POPs comparison with other cities was made. Agreements and commissions created by the Mexican government reduced OCPs emissions, however, more effort must be made to control PBDE emission sources.

Current situation of polycyclic aromatic hydrocarbons (PAH) in PM2.5 in a receptor site in Mexico City and estimation of carcinogenic PAH by combining non-real-time and real-time measurement techniques.

Air pollution is a public health concern. Polycyclic aromatic hydrocarbons (PAH) are ubiquitous atmospheric pollutants contained in the atmospheric aerosol. PAH in particulate matter with diameters ≤2.5 µm (PM2.5) represent a human health risk due to their toxic properties. In this study, PAH in PM2.5 at a receptor site of Mexico City during the dry cold season were determined. The most abundant PAH (median, 10-90th percentile, pg m-3) were benzo[ghi]perylene (467, 291-697), followed by pyrene (427, 218-642). A decrease around 40% in the carcinogenic PAH onto PM2.5 was calculated with respect to the same PAH measured a decade ago, at the same receptor site, despite of increase in vehicle fleet. The PAH decrease trend agrees with the decrease trend of CO, NO and NO2, released into the air by similar emission sources than PAH. Control emissions strategies implemented by local and federal authorities are discussed. PAH analyses were carried out by non-real-time and real-time methods. The PAH non-real-time method involved PM2.5 sampling, sample treatment and gas chromatography-mass spectrometry analysis. The PAH real-time method involved the use of a photoelectric aerosol sensor (PAS). The PAH determination by non-real time method was selective and efficient, with recoveries between 75 ±â€¯14% and 98 ±â€¯26%. By combining non-real-time and real-time methodologies, multivariate regression models were obtained based on PAS response, NO2 and wind speed to estimate PAH in PM2.5 at low-cost (r2 = 0.59 to r2 = 0.89). Fossil fuel combustion from vehicles was the major source around the sampling site. Diagnostic ratios (DR) based on retene, chrysene, and triphenylene, suggested biomass burning emission sources. Photo-oxidation in sunny months was observed based on benzo[a]pyrene, benzo[ghi]perylene, benz[a]anthracene, indeno[1,2,3-cd]pyrene and black carbon. The correlation analyses suggested transport of PM2.5, O3, BC and SO2 to the sampling site, and local emissions of PAH, NO and CO.

Aerial pesticide application causes DNA damage in pilots from Sinaloa, Mexico.

The use of pesticides in agricultural production originates residues in the environment where they are applied. Pesticide aerial application is a frequent source of exposure to pesticides by persons dedicated to agricultural practices and those living in neighboring communities of sprayed fields. The aim of the study was to assess the genotoxic effects of pesticides in workers occupationally exposed to these chemicals during their aerial application to agricultural fields of Sinaloa, Mexico. The study involved 30 pilots of airplanes used to apply pesticides via aerial application and 30 unexposed controls. Damage was evaluated through the micronucleus assay and by other nuclear abnormalities in epithelial cells of oral mucosa. The highest frequency ratios (FR) equal to 269.5 corresponded to binucleated cells followed by 54.2, corresponding to cells with pyknotic nuclei, 45.2 of cells with chromatin condensation, 3.7 of cells with broken-egg, 3.6 of cells with micronucleus, and 2.0 of karyolytic cells. Age, worked time, smoking, and alcohol consumption did not have significant influence on nuclear abnormalities in the pilots studied. Pesticide exposure was the main factor for nuclear abnormality results and DNA damage. Marked genotoxic damage was developed even in younger pilots with 2 years of short working period, caused by their daily occupational exposure to pesticides.

An innovative ultrasound assisted extraction micro-scale cell combined with gas chromatography/mass spectrometry in negative chemical ionization to determine persistent organic pollutants in air particulate matter.

New clean technologies are needed to determine concentration of organic pollutants without generating more pollution. A method to extract Persistent Organic Pollutants (POPs) from airborne particulate matter was developed using a novel technology recently patented called ultrasound assisted extraction micro-scale cell (UAE-MSC). This technology extracts, filters, collects the sample, and evaporates the solvent, on-line. No sample transfer is needed. The cell minimizes sample manipulation, solvent consumption, waste generation, time, and energy; fulfilling most of the analytical green chemistry protocol. The methodology was optimized applying a centred 23 factorial experimental design. Optimum conditions were used to validate and determine concentration of 16 organochlorine pesticides (OCls) and 6 polybrominated diphenyl ethers (PBDEs). The best conditions achieved were 2 extractions with 5mL (each) of dichloromethane over 5min (each) at 60°C and 80% ultrasound potency. POPs were determined by gas chromatography/mass spectrometry in negative chemical ionization (GC/MS-NCI). Analytical method validation was carried out on airborne particles spiked with POPs at seven concentration levels between 0.5 and 26.9pgm-3. This procedure was done by triplicate (N=21). Recovery, ranged between 65.5±2.3% and 107.5±3.0% for OCls and between 79.1±6.5% and 105.2±3.8% for PBDEs. Linearity (r2) was ≥0.94 for all compounds. Method detection limits, ranged from 0.5 to 2.7pgm-3, while limits of quantification (LOQ), ranged from 1.7 to 9.0pgm-3. A Bias from -18.6% to 9% for PBDEs was observed in the Standard Reference Material (SRM) 2787. SRM 2787 did not contain OCls. OCls recoveries were equivalent by UAE-MSC and Soxhlet methods UAE-MSC optimized extraction conditions reduced 30 times less solvent and decreased the extraction time from several hours to ten minutes, respect to Soxhlet. UAE-MSC was applied to 15 samples of particles less than 2.5µm (PM2.5) from three seasons (warm dry, rainy, and cold dry) collected in five sites around Mexico City. OCls (4,4'-DDE and endrin aldehyde) concentrations ranged from

Temporal variation of nitro-polycyclic aromatic hydrocarbons in PM10 and PM2.5 collected in Northern Mexico City.

With the aim to determine the presence of individual nitro-PAH contained in particles in the atmosphere of Mexico City, a monitoring campaign for particulate matter (PM(10) and PM(2.5)) was carried out in Northern Mexico City, from April 2006 to February 2007. The PM(10) annual median concentration was 65.2µgm(-3) associated to 7.6µgm(-3) of solvent-extractable organic matter (SEOM) corresponding to 11.4% of the PM(10) concentration and 38.6µgm(-3) with 5.9µgm(-3) SEOM corresponding to 15.2% for PM(2.5). PM concentration and SEOM varied with the season and the particle size. The quantification of nitro-polycyclic aromatic hydrocarbons (nitro-PAH) was developed through the standards addition method under two schemes: reference standard with and without matrix, the former giving the best results. The recovery percentages varied with the extraction method within the 52 to 97% range depending on each nitro-PAH. The determination of the latter was effected with and without sample purification, also termed fractioning, giving similar results. 8 nitro-PAH were quantified, and their sum ranged from 111 to 819pgm(-3) for PM(10) and from 58 to 383pgm(-3) for PM(2.5), depending on the season. The greatest concentration was for 9-Nitroanthracene in PM(10) and PM(2.5), detected during the cold-dry season, with a median (10th-90th percentiles) concentration in 235pgm(-3) (66-449pgm(-3)) for PM(10) and 73pgm(-3) (18-117pgm(-3)) for PM(2.5). The correlation among mass concentrations of the nitro-PAH and criteria pollutants was statistically significant for some nitro-PAH with PM(10), SEOM in PM(10), SEOM in PM(2.5), NO(X), NO(2) and CO, suggesting either sources, primary or secondary origin. The measured concentrations of nitro-PAH were higher than those reported in other countries, but lower than those from Chinese cities. Knowledge of nitro-PAH atmospheric concentrations can aid during the surveillance of diseases (cardiovascular and cancer risk) associated with these exposures.

Cell proliferation kinetics and genotoxicity in lymphocytes of smokers living in Mexico City.

Genotoxicity caused by tobacco smoke was assessed in peripheral blood lymphocytes of smokers living in Mexico City by determining sister chromatid exchange (SCE), cell proliferation kinetics (CPK), replication index (RI) and mitotic index (MI). Nicotine levels, and its major metabolite cotinine, were also estimated in urine samples using gas-chromatography-mass spectrometry to quantify smoking intensity. The outcome of the analysis and the comparison of the 77-smoker group with a non-smoking control group showed that moderate and heavy smokers exhibited significant differences (P < 0.001 and P < 0.05, respectively) in CPK, with an underlying delay in the cellular cycle; similarly, RI was significantly different in these groups (P < 0.001 and P < 0.0001, respectively). There were significant correlations (P < 0.05) between age and number of years the subject had been smoking, as well as between RI and nicotine and cotinine levels and between CPK (M1, M2 and M3) and nicotine and cotinine levels. Smokers were classified for the analysis according to the nicotine levels (it is in relation to number of cigarettes smoked per day) found in urine (ng/mL) as: light (10-250), moderate (251-850) and heavy (851-4110). Significant differences in CPK were found (P < 0.05) between moderate and heavy smokers and non-smokers. Significant differences in RI were found between moderate (P < 0.001) and heavy smokers (P < 0.0001) and non-smokers, but not for the light smoking group. MI was determined in 57 of the smokers, whereas SCE frequency was only recorded in 34 smokers. Both parameters yielded no significant differences, nor correlations with any of the assessed variables. In conclusion, cytokinetic and cytostatic effects were mainly detected in heavy and moderate smokers. Cell cycle delay and RI decrease were found in all ;healthy' smokers. The nicotine and cotinine exposure (causing oxidative damage to DNA) may have implications in the decrease in cell replication due to direct damage to DNA and/or a decrease in the DNA repair mechanisms. Alternatively, nicotine and cotinine may possibly induce apoptosis.