ABSTRACT
Benzophenone-3 (BP3) is a common ingredient in personal care products (PCPs) due to its well-established effectiveness in absorbing UV radiation. Sunscreen products are among the most widely used PCPs-containing BP3 applied to the skin, resulting in significant human exposure to BP3 primarily through a dermal application. In the present work, we have tested the action of three environmentally relevant concentrations of BP3 (2, 20 and 200 µg/L) on an in vitro model of implantation of murine blastocysts and on migration ability of the human trophoblast cell line Swan 71. We showed that BP3 caused a significant reduction of blastocyst expansion and a delayed hatching in a non-monotonic way. Besides, embryos displayed a delayed attachment in the three BP3 groups, resulting in a smaller implantation area on the 6th day of culture: BP3(2) (0.32 ± 0.07 mm2); BP3(20) (0.30 ± 0.08 mm2) and BP3(200) (0.25 ± 0.06 mm2) in comparison to the control (0.42 ± 0.07 mm2). We also found a reduced migration capacity of the human first-trimester trophoblast cell line Swan 71 in a scratch assay when exposed to BP3: the lowest dose displayed a higher uncovered area (UA) at 6h when compared to the control, whereas a higher UA of the wound was observed for the three BP3 concentrations at 18 and 24 h of exposure. The changes in UA provoked by BP3 restored to normal values in the presence of flutamide, an androgen receptor (AR) inhibitor. These results indicate that a direct impairment on early embryo implantation and a defective migration of extravillous trophoblast cells through the androgen receptor pathway can be postulated as mechanisms of BP3-action on early gestation with potential impact on fetal growth.
Subject(s)
Benzophenones , Cell Movement , Embryo Implantation , Sunscreening Agents , Trophoblasts , Ultraviolet Rays , Benzophenones/toxicity , Sunscreening Agents/toxicity , Sunscreening Agents/pharmacology , Trophoblasts/drug effects , Cell Movement/drug effects , Mice , Animals , Humans , Embryo Implantation/drug effects , Blastocyst/drug effects , Female , Cell LineABSTRACT
Previously, we found that the ultraviolet filter benzophenone-3 (BP3) causes fetal growth restriction in mice when is applied when implantation occurs (first week of gestation). However, whether BP3 can affect gestation and fertility after implantation period is unknown. We aimed to study the effects on reproductive physiology of the offspring caused by perinatal exposure to BP3. C57BL/6 pregnant mice were dermally exposed to 50 mg BP3/kg bw.day or olive oil (vehicle) from gestation day 9 (gd9) to postnatal day 21 (pnd1). We observed no differences in mother's weights, duration of gestation, number of pups per mother, onset of puberty or sex ratio. The weights of the pups exposed to benzophenone-3 were transiently lower than those of the control. Estrous cycle was not affected by perinatal exposure to BP3. Besides, we performed a fertility assessment by continuous breeding protocol: at 10 weeks of age, one F1 female and one F1 male mouse from each group was randomly chosen from each litter and housed together for a period of 6 months. We noticed a reduction in the number of deliveries per mother among dams exposed to BP3 during the perinatal period. To see if this decreased fertility could be associated to an early onset of oocytes depletion, we estimated the ovarian reserve of germ cells. We found reduced number of oocytes and primordial follicles in BP3. In conclusion, perinatal exposure to BP3 leads to a decline in the reproductive capacity of female mice in a continuous breeding protocol linked to oocyte depletion.
Subject(s)
Benzophenones , Mice, Inbred C57BL , Oocytes , Prenatal Exposure Delayed Effects , Animals , Female , Benzophenones/toxicity , Benzophenones/administration & dosage , Pregnancy , Male , Prenatal Exposure Delayed Effects/chemically induced , Oocytes/drug effects , Mice , Fertility/drug effects , Sunscreening Agents/toxicity , Maternal Exposure/adverse effectsABSTRACT
Urban wastewater reuse for agriculture provides reliable nutrient-rich water, reduces water stress, and strengthens food systems. However, wastewater reuse also presents health risks and characterizing the spatial dynamics of wastewater can help optimize risk mitigation. We conducted comparative risk analysis of exposure to wastewater in irrigation canals, where we compared those exposed to a) treated vs. untreated wastewater, and b) wastewater upstream vs. downstream from communities in the Mezquital Valley. The canal system with treated wastewater was sampled prior to being treated, directly after treatment, as well as before and after it flowed through a community. Along the canal system that carried untreated wastewater, we sampled before and after a community. We quantified the concentrations of bacterial, protozoal, and viral pathogens in the wastewater. Pathogen concentration data were used to calculate measures of relative risk between sampling points. Wastewater treatment reduced predicted bacterial pathogen infection risk in post-treatment locations (RR = 0.73, 95 % CI 0.61, 0.87), with no evidence of similar reductions in Giardia or viral pathogens (RR = 1.02, 95 % CI 0.56, 1.86 and RR = 1.18, 95 % CI 0.70, 2.02 respectively). Although infection risk decreased further down the canals, infection risk increased for bacterial pathogens after our sentinel community (RR = 1.94, 95 % 1.34, 2.86). For Giardia and viral pathogens infection risk was elevated but not significantly. We found similar evidence for increases in risk when comparing the treated section of the canal system with a canal section whose wastewater was not treated, i.e., the risk benefits of wastewater treatment were lost after our sentinel community for bacteria (RR = 5.27 vs. 2.08 for sampling points before and after our sentinel community respectively) and for Giardia (RR = 6.98 vs. 3.35 respectively). The increase in risk after transit through communities could have resulted from local community recontamination of the treated wastewater stream.
Subject(s)
Giardiasis , Wastewater , Humans , Mexico , Environment , Agriculture , Bacteria , GiardiaABSTRACT
Pubertal mammary branching morphogenesis is a hormone-regulated process susceptible to exposure to chemicals with endocrine disruptive capacity, such as the UV-filter benzophenone-3 (BP3). Our aim was to assess whether intrauterine or in vitro exposure to BP3 modified the branching morphogenesis of the female mouse mammary gland. For this, pregnant mice were dermally exposed to BP3 (0.15 or 50 mg/kg/day) from gestation day (GD) 8.5 to GD18.5. Sesame oil treatment served as control. Changes of the mammary glands of the offspring were studied on postnatal day 45. Further, mammary organoids from untreated mice were cultured under branching induction conditions and exposed for 9 days to BP3 (1 × 10-6 M, 1 × 10-9 M, or 1 × 10-12 M with 0.01% ethanol as control) to evaluate the branching progression. Mice that were exposed to BP3 in utero showed decreased mRNA levels of progesterone receptor (PR) and WNT4. However, estradiol and progesterone serum levels, mammary histomorphology, proliferation, and protein expression of estrogen receptor alpha (ESR1) and PR were not significantly altered. Interestingly, direct exposure to BP3 in vitro also decreased the mRNA levels of PR, RANKL, and amphiregulin without affecting the branching progression. Most effects were found after exposure to 50 mg/kg/day or 1 × 10-6 M of BP3, both related to sunscreen application in humans. In conclusion, exposure to BP3 does not impair mammary branching morphogenesis in our models. However, BP3 affects PR transcriptional expression and its downstream mediators, suggesting that exposure to BP3 might affect other developmental stages of the mammary gland.
Subject(s)
Benzophenones , Estradiol , Pregnancy , Humans , Mice , Female , Animals , Benzophenones/toxicity , Estradiol/metabolism , Morphogenesis , RNA, Messenger/metabolism , Mammary Glands, AnimalABSTRACT
Plant-based materials are an important source of bioactive compounds (BC) with interesting industrial applications. Therefore, adequate experimental strategies for maximizing their recovery yield are required. Among all procedures for extracting BC (maceration, Soxhlet, hydro-distillation, pulsed-electric field, enzyme, microwave, high hydrostatic pressure, and supercritical fluids), the ultrasound-assisted extraction (UAE) highlighted as an advanced, cost-efficient, eco-friendly, and sustainable alternative for recovering BC (polyphenols, flavonoids, anthocyanins, and carotenoids) from plant sources with higher yields. However, the UAE efficiency is influenced by several factors, including operational variables and extraction process (frequency, amplitude, ultrasonic power, pulse cycle, type of solvent, extraction time, solvent-to-solid ratio, pH, particle size, and temperature) that exert an impact on the molecular structures of targeted molecules, leading to variations in their biological properties. In this context, a diverse design of experiments (DOEs), including full or fractional factorial, Plackett-Burman, Box-Behnken, Central composite, Taguchi, Mixture, D-optimal, and Doehlert have been investigated alone and in combination to optimize the UAE of BC from plant-based materials, using the response surface methodology and mathematical models in a simple or multi-factorial/multi-response approach. The present review summarizes the advantages and limitations of the most common DOEs investigated to optimize the UAE of bioactive compounds from plant-based materials.
Subject(s)
Anthocyanins , Polyphenols , Flavonoids , Plant Extracts/chemistry , Solvents/chemistryABSTRACT
BACKGROUND: Satellite-based PM2.5 predictions are being used to advance exposure science and air-pollution epidemiology in developed countries; including emerging evidence about the impacts of PM2.5 on acute health outcomes beyond the cardiovascular and respiratory systems, and the potential modifying effects from individual-level factors in these associations. Research on these topics is lacking in low and middle income countries. We aimed to explore the association between short-term exposure to PM2.5 with broad-category and cause-specific mortality outcomes in the Mexico City Metropolitan Area (MCMA), and potential effect modification by age, sex, and SES characteristics in such associations. METHODS: We used a time-stratified case-crossover study design with 1,479,950 non-accidental deaths from the MCMA for the period of 2004-2019. Daily 1 × 1 km PM2.5 (median = 23.4 µg/m3; IQR = 13.6 µg/m3) estimates from our satellite-based regional model were employed for exposure assessment at the sub-municipality level. Associations between PM2.5 with broad-category (organ-system) and cause-specific mortality outcomes were estimated with distributed lag conditional logistic models. We also fit models stratifying by potential individual-level effect modifiers including; age, sex, and individual SES-related characteristics namely: education, health insurance coverage, and job categories. Odds ratios were converted into percent increase for ease of interpretation. RESULTS: PM2.5 exposure was associated with broad-category mortality outcomes, including all non-accidental, cardiovascular, cerebrovascular, respiratory, and digestive mortality. A 10-µg/m3 PM2.5 higher cumulative exposure over one week (lag06) was associated with higher cause-specific mortality outcomes including hypertensive disease [2.28% (95%CI: 0.26%-4.33%)], acute ischemic heart disease [1.61% (95%CI: 0.59%-2.64%)], other forms of heart disease [2.39% (95%CI: -0.35%-5.20%)], hemorrhagic stroke [3.63% (95%CI: 0.79%-6.55%)], influenza and pneumonia [4.91% (95%CI: 2.84%-7.02%)], chronic respiratory disease [2.49% (95%CI: 0.71%-4.31%)], diseases of the liver [1.85% (95%CI: 0.31%-3.41%)], and renal failure [3.48% (95%CI: 0.79%-6.24%)]. No differences in effect size of associations were observed between age, sex and SES strata. CONCLUSIONS: Exposure to PM2.5 was associated with non-accidental, broad-category and cause-specific mortality outcomes beyond the cardiovascular and respiratory systems, including specific death-causes from the digestive and genitourinary systems, with no indication of effect modification by individual-level characteristics.
Subject(s)
Air Pollutants , Air Pollution , Humans , Air Pollutants/adverse effects , Air Pollutants/analysis , Air Pollution/adverse effects , Air Pollution/analysis , Cross-Over Studies , Environmental Exposure/adverse effects , Environmental Exposure/analysis , Mexico/epidemiology , Particulate Matter/adverse effects , Particulate Matter/analysis , Male , FemaleABSTRACT
Worldwide, the fungus known as huitlacoche (Ustilago maydis (DC.) Corda) is a phytopathogen of maize plants that causes important economic losses in different countries. Conversely, it is an iconic edible fungus of Mexican culture and cuisine, and it has high commercial value in the domestic market, though recently there has been a growing interest in the international market. Huitlacoche is an excellent source of nutritional compounds such as protein, dietary fiber, fatty acids, minerals, and vitamins. It is also an important source of bioactive compounds with health-enhancing properties. Furthermore, scientific evidence shows that extracts or compounds isolated from huitlacoche have antioxidant, antimicrobial, anti-inflammatory, antimutagenic, antiplatelet, and dopaminergic properties. Additionally, the technological uses of huitlacoche include stabilizing and capping agents for inorganic nanoparticle synthesis, removing heavy metals from aqueous media, having biocontrol properties for wine production, and containing biosurfactant compounds and enzymes with potential industrial applications. Furthermore, huitlacoche has been used as a functional ingredient to develop foods with potential health-promoting benefits. The present review focuses on the biocultural importance, nutritional content, and phytochemical profile of huitlacoche and its related biological properties as a strategy to contribute to global food security through food diversification; moreover, the biotechnological uses of huitlacoche are also discussed with the aim of contributing to the use, propagation, and conservation of this valuable but overlooked fungal resource.
Subject(s)
Basidiomycota , Ustilago , Mexico , Dietary FiberABSTRACT
BACKGROUND: PM2.5 exposure has been associated with intima-media thickness (cIMT) increase. However, very few studies distinguished between left and right cIMT in relation to PM2.5 exposure. AIM: To evaluate associations between chronic exposure to PM2.5 and cIMT at bilateral, left, and right in adults from Mexico City. METHODS: This study comprised 913 participants from the control group, participants without personal or family history of cardiovascular disease, of the Genetics of Atherosclerosis Disease Mexican study (GEA acronym in Spanish), recruited at the Instituto Nacional de Cardiología Ignacio Chávez from June 2008 to January 2013. To assess the associations between chronic exposure to PM2.5 (per 5 µg/m3 increase) at different lag years (1-4 years) and cIMT (bilateral, left, and right) we applied distributed lag non-linear models (DLNMs). RESULTS: The median and interquartile range for cIMT at bilateral, left, and right, were 630 (555, 735), 640 (550, 750), and 620 (530, 720) µm, respectively. Annual average PM2.5 exposure was 26.64 µg/m3, with median and IQR, of 24.46 (23.5-25.46) µg/m3. Results from DLNMs adjusted for age, sex, body mass index, low-density lipoproteins, and glucose, showed that PM2.5 exposure for year 1 and 2, were positively and significantly associated with right-cIMT [6.99% (95% CI: 3.67; 10.42) and 2.98% (0.03; 6.01), respectively]. Negative associations were observed for PM2.5 at year 3 and 4 and right-cIMT; however only year 3 was statistically significant [-2.83% (95% CI: 5.12; -0.50)]. Left-cIMT was not associated with PM2.5 exposure at any lag year. The increase in bilateral cIMT followed a similar pattern as that observed for right-cIMT, but with lower estimates. CONCLUSIONS: Our results suggest different susceptibility between left and right cIMT associated with PM2.5 exposure highlighting the need of measuring both, left and right cIMT, regarding ambient air pollution in epidemiological studies.
Subject(s)
Air Pollution , Carotid Intima-Media Thickness , Environmental Exposure , Adult , Humans , Air Pollutants , Air Pollution/statistics & numerical data , Atherosclerosis/epidemiology , Body Mass Index , Environmental Exposure/statistics & numerical data , Mexico/epidemiology , Particulate MatterABSTRACT
BACKGROUND: Lead can affect early childhood development (ECD) differentially due to nutritional deficiencies that lead to stunted growth, defined as being at least two standard deviations below the average height-for-age. These deficiencies are more frequent among children living in rural locations or with lower socioeconomic status (SES); however, studies at a population level are scarce worldwide. Early childhood development plays a crucial role in influencing a child's health and wellbeing throughout life. Therefore, the aim of this study was to analyze how stunted growth can modify the association between lead exposure and ECD in children from disadvantaged communities. METHODS: Data were analyzed from the 2018 National Health and Nutrition Survey in localities with fewer than 100,000 inhabitants in Mexico (ENSANUT-100K). Capillary blood lead (BPb) levels were measured using a LeadCare II device and dichotomized as detectable (cutoff point ≥ 3.3 µg/dL) and non-detectable. As a measure of ECD, language development was assessed in n = 1394 children, representing 2,415,000 children aged 12-59 months. To assess the association between lead exposure and language z-scores, a linear model was generated adjusted by age, sex, stunted growth, maternal education, socioeconomic status, area, region (north, center, south), and family care characteristics; afterwards, the model was stratified by stunted growth. RESULTS: Fifty percent of children had detectable BPb and 15.3% had stunted growth. BPb showed a marginal inverse association with language z-scores (ß: -0.08, 95% CI: -0.53, 0.36). Children with detectable BPb and stunted growth had significantly lower language z-scores (ß: -0.40, 95% CI: -0.71, -0.10) than those without stunted growth (ß: -0.15, 95% CI: -0.36, 0.06). CONCLUSIONS: Children with stunted growth are more vulnerable to the adverse effects of lead exposure. These results add to previous research calling for action to reduce lead exposure, particularly in children with chronic undernutrition.
Subject(s)
Child Development , Lead , Child , Humans , Child, Preschool , Infant , Mexico/epidemiology , Lead/toxicity , Growth Disorders/epidemiology , Growth Disorders/etiology , Social ClassABSTRACT
Background: Satellite-based PM2.5 predictions are being used to advance exposure science and air-pollution epidemiology in developed countries; including emerging evidence about the impacts of PM2.5 on acute health outcomes beyond the cardiovascular and respiratory systems, and the potential modifying effects from individual-level factors in these associations. Research on these topics is lacking in Latin America. Methods: We used a time-stratified case-crossover study design with 1,479,950 non-accidental deaths from Mexico City Metropolitan Area for the period of 2004-2019. Daily 1×1 km PM2.5 (median=23.4 µg/m3; IQR=13.6 µg/m3) estimates from our satellite-based regional model were employed for exposure assessment at the sub-municipality level. Associations between PM2.5 with broad-category (organ-system) and cause-specific mortality outcomes were estimated with distributed lag conditional logistic models. We also fit models stratifying by potential individual-level effect modifiers including; age, sex, and individual SES-related characteristics namely: education, health insurance coverage, and job categories. Results: PM2.5 exposure was associated with higher total non-accidental, cardiovascular, cerebrovascular, respiratory, and digestive mortality. A 10-µg/m3 PM2.5 higher cumulative exposure over one week (lag06) was associated with higher cause-specific mortality outcomes including hypertensive disease [2.28% (95%CI: 0.26%-4.33%)], acute ischemic heart disease [1.61% (95%CI: 0.59%-2.64%)], other forms of heart disease [2.39% (95%CI: -0.35%-5.20%)], hemorrhagic stroke [3.63% (95%CI: 0.79%-6.55%)], influenza and pneumonia [4.91% (95%CI: 2.84%-7.02%)], chronic respiratory disease [2.49% (95%CI: 0.71%-4.31%)], diseases of the liver [1.85% (95%CI: 0.31%-3.41%)], and renal failure [3.48% (95%CI: 0.79%-6.24%)]. No differences in effect size of associations were observed between SES strata. Conclusions: Exposure to PM2.5 was associated with mortality outcomes beyond the cardiovascular and respiratory systems, including specific death-causes from the digestive and genitourinary systems, with no indications of effect modification by individual SES-related characteristics.
ABSTRACT
Lead (Pb), mercury (Hg), and manganese (Mn) are neurotoxic, but little is known about the neurodevelopmental effects associated with simultaneous prenatal exposure to these metals. We aimed to study the associations of Pb, Hg, and Mn prenatal levels (jointly and separately) with neurodevelopment in the first year of life. Methods: Pb, Hg, and Mn blood lead levels were measured in 253 pregnant women. Their offspring's neurodevelopment was assessed through the Bayley Scale of Infant Development III® at one, three, six, and twelve months. The metals' mean blood levels (µg/L) were Pb = 11.2, Hg = 2.1, and Mn = 10.2. Mean language, cognitive, and motor development scores of the infants at each age were between low-average and average. Multilevel models' results showed that language development coefficients of the offspring decreased by 1.5 points per 1 µg/dL increase in maternal blood lead levels (p = 0.002); the magnitude of the aforementioned association increased in children with maternal blood Mn < 9.6 µg/L (ß = -1.9, p = 0.003) or Hg > 1.9 µg/L (ß = -1.6, p = 0.013). Cognitive and motor development had negative associations with maternal blood Pb levels; the latter was statistically significant when the interaction term between Pb, Mn, and Hg was included (ß = -0.037, p = 0.03). Prenatal exposure to low Pb levels may impair infants' neurodevelopment in the first year of life, even more so if they are exposed to Hg or deficient in Mn.
Subject(s)
Mercury , Prenatal Exposure Delayed Effects , Infant , Child , Female , Humans , Pregnancy , Lead/toxicity , Mercury/toxicity , Manganese/toxicity , Prenatal Exposure Delayed Effects/epidemiology , IonsABSTRACT
The Latin America and the Caribbean (LAC) region makes up 8.4% of the world's population. Human biomonitoring (HBM) programs, which can shed light on population-level exposure to environmental contaminants such as toxic metals and thus, improve the health of the populations are inexistent in LAC countries. We call for the creation of HBM programs in the region and identify three viable design options for HBM at the individual level, through national surveys, newborn blood collection, and biobanks. We highlight some of challenges to the implementation of HBM programs, including financial and human resources, technical constrains (laboratory), sample, and data logistics. Finally, we provide the case studies of Brazil, Chile, Mexico, and Uruguay, to illustrate a range of responses to toxic metal exposure in non-occupational populations. Although different in many respects, the individual country responses share two commonalities: 1) academic centers drive the research to raise awareness of governmental entities; 2) reference levels are adapted from international norms rather than arising from the studied populations. Well-designed and sufficiently funded biomonitoring systems need to be established in each country of the LAC region. HBM programs are key to promoting human health by informing the public and contributing to policy processes that establish sustainable environmental controls and health prevention programs.
Subject(s)
Metalloids , Biological Monitoring , Caribbean Region , Humans , Infant, Newborn , Latin America , MexicoABSTRACT
BACKGROUND: Machine-learning algorithms are becoming popular techniques to predict ambient air PM2.5 concentrations at high spatial resolutions (1 × 1 km) using satellite-based aerosol optical depth (AOD). Most machine-learning models have aimed to predict 24 h-averaged PM2.5 concentrations (mean PM2.5) in high-income regions. Over Mexico, none have been developed to predict subdaily peak levels, such as the maximum daily 1-h concentration (max PM2.5). OBJECTIVE: Our goal was to develop a machine-learning model to predict mean PM2.5 and max PM2.5 concentrations in the Mexico City Metropolitan Area from 2004 through 2019. METHODS: We present a new modeling approach based on extreme gradient boosting (XGBoost) and inverse-distance weighting that uses AOD, meteorology, and land-use variables. We also investigated applications of our mean PM2.5 predictions that can aid local authorities in air-quality management and public-health surveillance, such as the co-occurrence of high PM2.5 and heat, compliance with local air-quality standards, and the relationship of PM2.5 exposure with social marginalization. RESULTS: Our models for mean and max PM2.5 exhibited good performance, with overall cross-validated mean absolute errors (MAE) of 3.68 and 9.20 µg/m3, respectively, compared to mean absolute deviations from the median (MAD) of 8.55 and 15.64 µg/m3. In 2010, everybody in the study region was exposed to unhealthy levels of PM2.5. Hotter days had greater PM2.5 concentrations. Finally, we found similar exposure to PM2.5 across levels of social marginalization. SIGNIFICANCE: Machine learning algorithms can be used to predict highly spatiotemporally resolved PM2.5 concentrations even in regions with sparse monitoring. IMPACT: Our PM2.5 predictions can aid local authorities in air-quality management and public-health surveillance, and they can advance epidemiological research in Central Mexico with state-of-the-art exposure assessment methods.
Subject(s)
Machine Learning , Meteorology , Humans , MexicoABSTRACT
Available data on the acute cardiovascular effect of ambient air pollution (AAP) in Latin America is limited considering that over 80% of its 1 billion inhabitants live in urban settlements with poor air quality. The study aim was to evaluate the association between Cardiovascular Emergency Department Visits (CEDVs) and AAP in Mexico City from 2016 to 2019 using generalized additive models with distributed lags to examine the percentage change of CEDVs and a backward approach of time-series model to calculate attributable fractions. A total of 48,891 CEDVs were recorded in a period of 1019 days. We estimated a significant percentage increase for each 10 µg/m3 of PM10 at Lag0-5 (2.8%, 95%CI 0.6-5.0), PM2.5 at Lag0-6 (3.7%, 95%CI 0.1-7.6), O3 at Lag0-5 (1.1%, 95%CI 0.2-2.0), NO2 at Lag0-4 (2.5%, 95%CI 0.3-4.7) and for each 1 mg/m3 of CO at Lag0 (6.6%, 95%CI 0.3-13.2). Overall, 10.3% of CEDVs in Mexico City may be related to PM10 exposure, 9.5% to PM2.5, 10.3% to O3, 11% to NO2 and 5.7% to CO. AAP significantly increase cardiovascular morbidity impacting on emergency medical services.
Subject(s)
Air Pollutants , Air Pollution , Environmental Pollutants , Air Pollutants/analysis , Air Pollutants/toxicity , Air Pollution/analysis , China , Emergency Service, Hospital , Environmental Exposure/analysis , Mexico/epidemiology , Particulate Matter/analysis , Particulate Matter/toxicityABSTRACT
BACKGROUND: Air pollution is a risk factor for type 2 diabetes (T2D). However, scarse longitudinal studies have evaluated this association in low- and middle-income countries, where 80% of the worldwide cases of T2D occur. OBJECTIVE: Our aim was to estimate the association between PM2.5 and NO2 exposure and incident T2D, in the Mexican Teachers' Cohort (MTC). METHODS: We selected a subsample of female teachers from the MTC from Mexico City metropolitan area (MCMA), recruited in 2008 and with active follow-up every three years. We assigned the monthly time-weighted exposures (PM2.5 and NO2) using home and work addresses, until failure, censoring or death. We developed two high resolution (1 × 1-km) spatiotemporal predictive generalized additive models of PM2.5 and NO2. Incident diabetes was identified through self-report and two administrative databases of registered diabetes patients. We fitted time-varying Cox models to estimate hazard ratios of the relation between PM2.5 and NO2 and incident T2D, adjusting for confounding variables that were identified using a causal model. RESULTS: A total of 13,669 teachers were followed-up for a maximum of 11.5 years, over which 996 incident T2D cases (88 cases per 100,000 person-months) occurred. Incident T2D increased by 72% (HR = 1.72 [1.47-2.01]) for each 10 µg/m3 increase of PM2.5, and 52% for each 10 ppb of NO2 (HR = 1.52 [1.37-1.68]). DISCUSSION: Mid-term exposure to PM2.5 and NO2 was associated with a higher risk of T2D after adjusting for indoor wood smoke, socioeconomic status, and physical activity. These associations were attenuated in two-pollutant models but remained positive when evaluated long-term exposure. This is the first prospective study to evaluate T2D risk by exposure to both pollutants, PM2.5 and NO2 in a population from an upper middle-income country in the Americas.
Subject(s)
Air Pollutants , Air Pollution , Diabetes Mellitus, Type 2 , Air Pollutants/analysis , Air Pollution/analysis , Diabetes Mellitus, Type 2/epidemiology , Environmental Exposure/analysis , Female , Humans , Incidence , Mexico/epidemiology , Particulate Matter/analysis , Prospective StudiesABSTRACT
OBJECTIVES: We designed and conducted a narrative review consistent with the PRISMA guidelines (PROSPERO registration number: CRD42018099498) to evaluate the association between environmental metals (manganese, mercury, iron) and Parkinson's Disease (PD) in low and middle-income countries (LMIC). METHODS: Data sources: A total of 19 databases were screened, and 2,048 references were gathered. Study selection: Randomized controlled trials, cluster trials, cohort studies, case-control studies, nested case-control studies, ecological studies, cross-sectional studies, case series, and case reports carried out in human adults of LMIC, in which the association between at least one of these three metals and the primary outcome were reported. Data extraction: We extracted qualitative and quantitative data. The primary outcome was PD cases, defined by clinical criteria. A qualitative analysis was conducted. RESULTS: Fourteen observational studies fulfilled the selection criteria. Considerable variation was observed between these studies' methodologies for the measurement of metal exposure and outcome assessment. A fraction of studies suggested an association between the exposure and primary outcome; nevertheless, these findings should be weighted and appraised on the studies' design and its implementation limitations, flaws, and implications. CONCLUSIONS: Further research is required to confirm a potential risk of metal exposure and its relationship to PD. To our awareness, this is the first attempt to evaluate the association between environmental and occupational exposure to metals and PD in LMIC settings using the social determinants of health as a framework.
Subject(s)
Environmental Exposure , Metals, Heavy , Occupational Exposure , Parkinson Disease , Cross-Sectional Studies , Developing Countries , Environmental Exposure/adverse effects , Humans , Iron/toxicity , Manganese/toxicity , Mercury/toxicity , Metals, Heavy/toxicity , Occupational Exposure/adverse effects , Parkinson Disease/epidemiologyABSTRACT
Health effects related to exposure to air pollution such as ozone (O3) have been documented. The World Health Organization has recommended the use of the Sum of O3 Means Over 35 ppb (SOMO35) to perform Health Impact Assessments (HIA) for long-term exposure to O3. We estimated the avoidable mortality associated with long-term exposure to tropospheric O3 in 14 cities in Mexico using information for 2015. The economic valuation of avoidable deaths related to SOMO35 exposure was performed using the willingness to pay (WTP) and human capital (HC) approaches. We estimated that 627 deaths (95% uncertainty interval (UI): 227-1051) from respiratory diseases associated with the exposure to O3 would have been avoided in people over 30 years in the study area, which confirms the public health impacts of ambient air pollution. The avoidable deaths account for almost 1400 million USD under the WTP approach, whilst the HC method yielded a lost productivity estimate of 29.7 million USD due to premature deaths. Our findings represent the first evidence of the health impacts of O3 exposure in Mexico, using SOMO35 metrics.
Subject(s)
Air Pollutants , Air Pollution , Ozone , Air Pollutants/analysis , Air Pollutants/toxicity , Air Pollution/analysis , Air Pollution/statistics & numerical data , Environmental Exposure , Humans , Mexico/epidemiology , Ozone/analysis , Ozone/toxicity , Particulate Matter/analysisABSTRACT
Background: Little is known about the potential impact of climate change on food systems and diet. We aimed to estimate the association of changes in rainfall and temperatures with consumption of unprocessed and processed foods among residents of Mexican cities by climate region. Methods: We analyzed 3,312 participants of the 2012 Mexican National Health and Nutrition Survey with dietary intake and sociodemographic information linked to historical rainfall and temperature data collected by the Mexican National Weather Service. We classified foods as unprocessed, processed, or ultra-processed. We performed multilevel linear regression to estimate the association of annual change in rainfalls (for each 0.5 mm decrease) and temperatures (for each 0.1°C increase) at municipality level over the past 5 years with consumption of processed and unprocessed foods measured as the contribution to total energy intake. We investigated whether associations differed by climate region (tropical, temperate, and arid). Results: Each 0.5 mm annual decrease in precipitation was associated with lower consumption of unprocessed foods and higher consumption of ultra-processed foods [mean differences in percent contribution to total energy intake -0.009% (95% CI: -0.019, < -0.001) and 0.011% (95% CI: 0.001, 0.021), respectively]. Each 0.1 degree Celsius annual increase in temperature was also associated with lower consumption of unprocessed and higher consumption of ultra-processed foods [mean differences in percent contribution to total energy intake was -0.03 (95% CI: -0.05, -0.01) and 0.03% (95% CI: <0.01, 0.05)]. When stratified by climate region these associations were only observed in tropical regions. Conclusions: Decreases in rainfalls and increases in temperature were associated with lower consumption of unprocessed foods but higher consumption of ultra-processed foods, especially in tropical regions. Previous studies have established how food production affects the climate, our study suggests that climate change could, in turn, reinforce modern food production, closing a vicious circle with clear negative implications for planetary health.
ABSTRACT
Chlorpyrifos (CPF), the most used insecticide in Argentina, can act as an endocrine disruptor at low doses. We previously demonstrated that chronic exposure to CPF induces hormonal imbalance in vivo. The aim of this work was to study the effects of low concentrations of CPF (0.01 and 1 mg/kg/day) on the reproductive system of virgin adult rats. In the ovary, we studied the effects of CPF on steroidogenesis by determining steroid hormone content by RIA and CYP11 and CYP19 enzyme expression by qRT-PCR. The estrous cycle was evaluated by microscopic observation of vaginal smear, as well as by changes in uterine histology. In endometrium, we determined the fractal dimension and expression of PCNA, ERα and PR by IHC. Our results showed that chronic exposure to CPF affects ovarian steroid synthesis, causing alterations in the normal cyclicity of animals. In addition, CPF induced proliferative changes in the uterus, suggesting that it could affect reproduction or act as a risk factor in the development of uterine proliferative pathologies.
Subject(s)
Chlorpyrifos/administration & dosage , Chlorpyrifos/toxicity , Estrous Cycle/drug effects , Ovary/drug effects , Uterus/drug effects , Animals , Dose-Response Relationship, Drug , Drug Administration Schedule , Female , Insecticides/administration & dosage , Insecticides/toxicity , Random Allocation , Rats , Rats, Sprague-Dawley , Vagina/drug effectsABSTRACT
Resumen: Objetivo: Analizar la asociación entre la exposición crónica a contaminantes atmosféricos y la tasa de mortalidad por Covid-19 en ciudades mexicanas. Material y métodos: Estudio ecológico en 25 ciudades mexicanas utilizando el reporte de casos diarios de muertes por Covid-19 (febrero a junio 2020) y datos validados de contaminantes atmosféricos, considerando concentraciones promedio en cada ciudad en el último año. Se utilizaron modelos de regresión Poisson, con modelos aditivos generalizados y variables de ajuste. Resultados: Se encontró un incremento significativo de 3.5% (IC95% 2.3-4.7) en la tasa de mortalidad por Covid-19 por incremento de 1µg/m3 de NO2. La asociación con PM2.5 fue no significativa, con un incremento de 1.8% por cada µg/m3. Conclusiones: Los resultados sugieren una asociación entre la mortalidad por Covid-19 y la exposición a NO2. Esta primera aproximación del riesgo asociado con la contaminación del aire requiere de análisis más precisos, pero es consistente con estudios de otras regiones.
Abstract Objective: To analyze the relationship between chronic exposures to air pollution with Covid-19 death rate in Mexican cities. Materials and methods: Ecological study in 25 Mexican cities using the report of daily Covid-19 deaths (from February to June 2020) and validated data of air pollutants, considering average concentrations in each city for the last year. Poisson regression models using generalized additive models with adjustment variables (GAM) were used. Results: A significant increase of 3.5% (95% CI 2.3-4.7) was found in Covid-19 death rate for each 1µg/m3 in annual concentration of NO2. The association with PM2.5 was not significant, with an increase of 1.8% for each 1µg/m3. Conclusions: Results suggest an association between Covid-19 mortality and chronic exposure to NO2. This first approximation of the risk associated with air pollution requires a more precise analysis, but is consistent with what was observed in other studies.