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A recent epidemic of malaria in the highlands of Bolivia and establishment of multiple Anopheles species mosquitoes in the highlands of Ecuador highlights the reemergence of malaria in the Andes Mountains in South America. Because malaria was endemic to many highland valleys at the beginning of the 20th century, this review outlines the 20th century history of malaria in the highlands of Ecuador, and focuses on its incidence (e.g., geographic distribution) and elimination from the northern highland valleys of Pichincha and Imbabura and the role of the Guayaquil to Quito railway in creating highland larval habitat and inadvertently promoting transportation of the vector and parasite. Involvement of control organizations in combating malaria in Ecuador is also outlined in a historical context. [ABSTRACT FROM AUTHOR]

Introduction: Mortality is associated with long-term exposure to fine particulate matter (particulate matter ≤2.5 μm in aerodynamic diameter; PM 2.5 ), although the magnitude and form of these associations remain poorly understood at lower concentrations. Knowledge gaps include the shape of concentration-response curves and the lowest levels of exposure at which increased risks are evident and the occurrence and extent of associations with specific causes of death. Here, we applied improved estimates of exposure to ambient PM 2.5 to national population-based cohorts in Canada, including a stacked cohort of 7.1 million people who responded to census year 1991, 1996, or 2001. The characterization of the shape of the concentration-response relationship for nonaccidental mortality and several specific causes of death at low levels of exposure was the focus of the Mortality-Air Pollution Associations in Low Exposure Environments (MAPLE) Phase 1 report. In the Phase 1 report we reported that associations between outdoor PM 2.5 concentrations and nonaccidental mortality were attenuated with the addition of ozone (O 3 ) or a measure of gaseous pollutant oxidant capacity (O x ), which was estimated from O 3 and nitrogen dioxide (NO 2 ) concentrations. This was motivated by our interests in understanding both the effects air pollutant mixtures may have on mortality and also the role of O 3 as a copollutant that shares common sources and precursor emissions with those of PM 2.5 . In this Phase 2 report, we further explore the sensitivity of these associations with O 3 and O x , evaluate sensitivity to other factors, such as regional variation, and present ambient PM 2.5 concentration-response relationships for specific causes of death., Methods: PM 2.5 concentrations were estimated at 1 km 2 spatial resolution across North America using remote sensing of aerosol optical depth (AOD) combined with chemical transport model (GEOS-Chem) simulations of the AOD:surface PM 2.5 mass concentration relationship, land use information, and ground monitoring. These estimates were informed and further refined with collocated measurements of PM 2.5 and AOD, including targeted measurements in areas of low PM 2.5 concentrations collected at five locations across Canada. Ground measurements of PM 2.5 and total suspended particulate matter (TSP) mass concentrations from 1981 to 1999 were used to backcast remote-sensing-based estimates over that same time period, resulting in modeled annual surfaces from 1981 to 2016., Annual exposures to PM 2.5 were then estimated for subjects in several national population-based Canadian cohorts using residential histories derived from annual postal code entries in income tax files. These cohorts included three census-based cohorts: the 1991 Canadian Census Health and Environment Cohort (CanCHEC; 2.5 million respondents), the 1996 CanCHEC (3 million respondents), the 2001 CanCHEC (3 million respondents), and a Stacked CanCHEC where duplicate records of respondents were excluded (Stacked CanCHEC; 7.1 million respondents). The Canadian Community Health Survey (CCHS) mortality cohort (mCCHS), derived from several pooled cycles of the CCHS (540,900 respondents), included additional individual information about health behaviors. Follow-up periods were completed to the end of 2016 for all cohorts. Cox proportional hazard ratios (HRs) were estimated for nonaccidental and other major causes of death using a 10-year moving average exposure and 1-year lag. All models were stratified by age, sex, immigrant status, and where appropriate, census year or survey cycle. Models were further adjusted for income adequacy quintile, visible minority status, Indigenous identity, educational attainment, labor-force status, marital status, occupation, and ecological covariates of community size, airshed, urban form, and four dimensions of the Canadian Marginalization Index (Can-Marg; instability, deprivation, dependency, and ethnic concentration). The mCCHS analyses were also adjusted for individual-level measures of smoking, alcohol consumption, fruit and vegetable consumption, body mass index (BMI), and exercise behavior., In addition to linear models, the shape of the concentration-response function was investigated using restricted cubic splines (RCS). The number of knots were selected by minimizing the Bayesian Information Criterion (BIC). Two additional models were used to examine the association between nonaccidental mortality and PM 2.5 . The first is the standard threshold model defined by a transformation of concentration equaling zero if the concentration was less than a specific threshold value and concentration minus the threshold value for concentrations above the threshold. The second additional model was an extension of the Shape Constrained Health Impact Function (SCHIF), the eSCHIF, which converts RCS predictions into functions potentially more suitable for use in health impact assessments. Given the RCS parameter estimates and their covariance matrix, 1,000 realizations of the RCS were simulated at concentrations from the minimum to the maximum concentration, by increments of 0.1 μg/m 3 . An eSCHIF was then fit to each of these RCS realizations. Thus, 1,000 eSCHIF predictions and uncertainty intervals were determined at each concentration within the total range., Sensitivity analyses were conducted to examine associations between PM 2.5 and mortality when in the presence of, or stratified by tertile of, O 3 or O x . Additionally, associations between PM 2.5 and mortality were assessed for sensitivity to lower concentration thresholds, where person-years below a threshold value were assigned the mean exposure within that group. We also examined the sensitivity of the shape of the nonaccidental mortality-PM 2.5 association to removal of person-years at or above 12 μg/m 3 (the current U.S. National Ambient Air Quality Standard) and 10 μg/m 3 (the current Canadian and former [2005] World Health Organization [WHO] guideline, and current WHO Interim Target-4). Finally, differences in the shapes of PM 2.5 -mortality associations were assessed across broad geographic regions (airsheds) within Canada., Results: The refined PM 2.5 exposure estimates demonstrated improved performance relative to estimates applied previously and in the MAPLE Phase 1 report, with slightly reduced errors, including at lower ranges of concentrations (e.g., for PM 2.5 <10 μg/m 3 )., Positive associations between outdoor PM 2.5 concentrations and nonaccidental mortality were consistently observed in all cohorts. In the Stacked CanCHEC analyses (1.3 million deaths), each 10-μg/m 3 increase in outdoor PM 2.5 concentration corresponded to an HR of 1.084 (95% confidence interval [CI]: 1.073 to 1.096) for nonaccidental mortality. For an interquartile range (IQR) increase in PM 2.5 mass concentration of 4.16 μg/m 3 and for a mean annual nonaccidental death rate of 92.8 per 10,000 persons (over the 1991-2016 period for cohort participants ages 25-90), this HR corresponds to an additional 31.62 deaths per 100,000 people, which is equivalent to an additional 7,848 deaths per year in Canada, based on the 2016 population. In RCS models, mean HR predictions increased from the minimum concentration of 2.5 μg/m 3 to 4.5 μg/m 3 , flattened from 4.5 μg/m 3 to 8.0 μg/m 3 , then increased for concentrations above 8.0 μg/m 3 . The threshold model results reflected this pattern with -2 log-likelihood values being equal at 2.5 μg/m 3 and 8.0 μg/m 3 . However, mean threshold model predictions monotonically increased over the concentration range with the lower 95% CI equal to one from 2.5 μg/m 3 to 8.0 μg/m 3 . The RCS model was a superior predictor compared with any of the threshold models, including the linear model., In the mCCHS cohort analyses inclusion of behavioral covariates did not substantially change the results for both linear and nonlinear models. We examined the sensitivity of the shape of the nonaccidental mortality-PM 2.5 association to removal of person-years at or above the current U.S. and Canadian standards of 12 μg/m 3 and 10 μg/m 3 , respectively. In the full cohort and in both restricted cohorts, a steep increase was observed from the minimum concentration of 2.5 μg/m 3 to 5 μg/m 3 . For the full cohort and the <12 μg/m 3 cohort the relationship flattened over the 5 to 9 μg/m 3 range and then increased above 9 μg/m 3 . A similar increase was observed for the <10 μg/m 3 cohort followed by a clear decline in the magnitude of predictions over the 5 to 9 μg/m 3 range and an increase above 9 μg/m 3 . Together these results suggest that a positive association exists for concentrations >9 μg/m 3 with indications of adverse effects on mortality at concentrations as low as 2.5 μg/m 3 ., Among the other causes of death examined, PM 2.5 exposures were consistently associated with an increased hazard of mortality due to ischemic heart disease, respiratory disease, cardiovascular disease, and diabetes across all cohorts. Associations were observed in the Stacked CanCHEC but not in all other cohorts for cerebrovascular disease, pneumonia, and chronic obstructive pulmonary disease (COPD) mortality. No significant associations were observed between mortality and exposure to PM 2.5 for heart failure, lung cancer, and kidney failure., In sensitivity analyses, the addition of O 3 and O x attenuated associations between PM 2.5 and mortality. When analyses were stratified by tertiles of copollutants, associations between PM 2.5 and mortality were only observed in the highest tertile of O 3 or O x . Across broad regions of Canada, linear HR estimates and the shape of the eSCHIF varied substantially, possibly reflecting underlying differences in air pollutant mixtures not characterized by PM 2.5 mass concentrations or the included gaseous pollutants. Sensitivity analyses to assess regional variation in population characteristics and access to healthcare indicated that the observed regional differences in concentration-mortality relationships, specifically the flattening of the concentration-mortality relationship over the 5 to 9 μg/m 3 range, was not likely related to variation in the makeup of the cohort or its access to healthcare, lending support to the potential role of spatially varying air pollutant mixtures not sufficiently characterized by PM 2.5 mass concentrations., Conclusions: In several large, national Canadian cohorts, including a cohort of 7.1 million unique census respondents, associations were observed between exposure to PM 2.5 with nonaccidental mortality and several specific causes of death. Associations with nonaccidental mortality were observed using the eSCHIF methodology at concentrations as low as 2.5 μg/m 3 , and there was no clear evidence in the observed data of a lower threshold, below which PM 2.5 was not associated with nonaccidental mortality., (© 2022 Health Effects Institute. All rights reserved.)

Background: Associations between mortality and exposure to ambient air pollution are usually explored using concentrations of residential outdoor fine particulate matter (PM 2.5 ) to estimate individual exposure. Such studies all have an important limitation in that they do not capture data on individual mobility throughout the day to areas where concentrations may be substantially different, leading to possible exposure misclassification. We examine the possible role of outdoor PM 2.5 concentrations at work for a large population-based mortality cohort., Methods: Using the 2001 Canadian Census Health and Environment Cohort (CanCHEC), we created a time-weighted average that incorporates employment hours worked in the past week and outdoor PM 2.5 concentration at work and home. We used a Cox proportional hazard model with a 15-year follow-up (2001 to 2016) to explore whether inclusion of workplace estimates had an impact on hazard ratios for mortality for this cohort., Results: Hazard ratios relying on outdoor PM 2.5 concentration at home were not significantly different from those using a time-weighted estimate, for the full cohort, nor for those who commute to a regular workplace. When exploring cohort subgroups according to neighborhood type and commute distance, there was a notable but insignificant change in risk of nonaccidental death for those living in car-oriented neighborhoods, and with commutes greater than 10 km., Conclusions: Risk analyses performed with large cohorts in low-pollution environments do not seem to be biased if relying solely on outdoor PM 2.5 concentrations at home to estimate exposure., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report., (Copyright © 2021 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)

Background: Approximately 2.9 million deaths are attributed to ambient fine particle air pollution around the world each year (PM 2.5 ). In general, cohort studies of mortality and outdoor PM 2.5 concentrations have limited information on individuals exposed to low levels of PM 2.5 as well as covariates such as smoking behaviours, alcohol consumption, and diet which may confound relationships with mortality. This study provides an updated and extended analysis of the Canadian Community Health Survey-Mortality cohort: a population-based cohort with detailed PM 2.5 exposure data and information on a number of important individual-level behavioural risk factors. We also used this rich dataset to provide insight into the shape of the concentration-response curve for mortality at low levels of PM 2.5 ., Methods: Respondents to the Canadian Community Health Survey from 2000 to 2012 were linked by postal code history from 1981 to 2016 to high resolution PM 2.5 exposure estimates, and mortality incidence to 2016. Cox proportional hazard models were used to estimate the relationship between non-accidental mortality and ambient PM 2.5 concentrations (measured as a three-year average with a one-year lag) adjusted for socio-economic, behavioural, and time-varying contextual covariates., Results: In total, 50,700 deaths from non-accidental causes occurred in the cohort over the follow-up period. Annual average ambient PM 2.5 concentrations were low (i.e. 5.9 μg/m 3 , s.d. 2.0) and each 10 μg/m 3 increase in exposure was associated with an increase in non-accidental mortality (HR = 1.11; 95% CI 1.04-1.18). Adjustment for behavioural covariates did not materially change this relationship. We estimated a supra-linear concentration-response curve extending to concentrations below 2 μg/m 3 using a shape constrained health impact function. Mortality risks associated with exposure to PM 2.5 were increased for males, those under age 65, and non-immigrants. Hazard ratios for PM 2.5 and mortality were attenuated when gaseous pollutants were included in models., Conclusions: Outdoor PM 2.5 concentrations were associated with non-accidental mortality and adjusting for individual-level behavioural covariates did not materially change this relationship. The concentration-response curve was supra-linear with increased mortality risks extending to low outdoor PM 2.5 concentrations.

Background: Ambient fine particulate air pollution with aerodynamic diameter ≤ 2.5   μ m ( PM 2.5 ) is an important contributor to the global burden of disease. Information on the shape of the concentration-response relationship at low concentrations is critical for estimating this burden, setting air quality standards, and in benefits assessments., Objectives: We examined the concentration-response relationship between PM 2.5 and nonaccidental mortality in three Canadian Census Health and Environment Cohorts (CanCHECs) based on the 1991, 1996, and 2001 census cycles linked to mobility and mortality data., Methods: Census respondents were linked with death records through 2016, resulting in 8.5 million adults, 150 million years of follow-up, and 1.5 million deaths. Using annual mailing address, we assigned time-varying contextual variables and 3-y moving-average ambient PM 2.5 at a 1 × 1   km spatial resolution from 1988 to 2015. We ran Cox proportional hazards models for PM 2.5 adjusted for eight subject-level indicators of socioeconomic status, seven contextual covariates, ozone, nitrogen dioxide, and combined oxidative potential. We used three statistical methods to examine the shape of the concentration-response relationship between PM 2.5 and nonaccidental mortality., Results: The mean 3-y annual average estimate of PM 2.5 exposure ranged from 6.7 to 8.0   μ g / m 3 over the three cohorts. We estimated a hazard ratio (HR) of 1.053 [95% confidence interval (CI): 1.041, 1.065] per 10 - μ g / m 3 change in PM 2.5 after pooling the three cohort-specific hazard ratios, with some variation between cohorts (1.041 for the 1991 and 1996 cohorts and 1.084 for the 2001 cohort). We observed a supralinear association in all three cohorts. The lower bound of the 95% CIs exceeded unity for all concentrations in the 1991 cohort, for concentrations above 2   μ g / m 3 in the 1996 cohort, and above 5   μ g / m 3 in the 2001 cohort., Discussion: In a very large population-based cohort with up to 25 y of follow-up, PM 2.5 was associated with nonaccidental mortality at concentrations as low as 5   μ g / m 3 . https://doi.org/10.1289/EHP5204.

Outdoor fine particulate air pollution (PM 2.5 ) is known to increase mortality risk and is recognized as an important contributor to global disease burden. However, less is known about how oxidant gases may modify the chronic health effects of PM 2.5 . In this study, we examined how the oxidant capacity of O 3 and NO 2 (using a redox-weighted average, O x ) may modify the relationship between PM 2.5 and mortality in the 2001 Canadian Census Health and Environment Cohort. In total, 2,448,500 people were followed over a 10.6-year period. Each 3.86 µg/m 3 increase in PM 2.5 was associated with nonaccidental (Hazard Ratio (HR) = 1.095, 95% CI: 1.077, 1.112), cardiovascular (HR = 1.088, 95% CI: 1.059, 1.118), and respiratory mortality (HR = 1.110, 95% CI: 1.051, 1.171) in the highest tertile of O x whereas weaker/null associations were observed in the middle and lower tertiles. Analysis of joint non-linear concentration-response relationships for PM 2.5 and O x suggested threshold concentrations between approximately 23 and 25 ppb with O x concentrations above these values strengthening PM 2.5 -mortality associations. Overall, our findings suggest that oxidant gases enhance the chronic health risks of PM 2.5 . In some areas, reductions in O x concentrations may have the added benefit of reducing the public health impacts of PM 2.5 even if mass concentrations remain unchanged.

Background: Large cohort studies have been used to characterise the association between long-term exposure to fine particulate matter (PM 2.5 ) air pollution with non-accidental, and cause-specific mortality. However, there has been no consensus as to the shape of the association between concentration and response., Methods: To examine the shape of this association, we developed a new cohort based on respondents to the 2001 Canadian census long-form. We applied new annual PM 2.5 concentration estimates based on remote sensing and ground measurements for Canada at a 1km spatial scale from 1998 to 2011. We followed 2.4 million respondents who were non-immigrants aged 25-90 years and did not reside in an institution over a 10 year period for mortality. Exposures were assigned as a 3-year mean prior to the follow-up year. Income tax files were used to account for residential mobility among respondents using postal codes, with probabilistic imputation used for missing postal codes in the tax data. We used Cox survival models to determine hazard ratios (HRs) for cause-specific mortality. We also estimated Shape Constrained Health Impact Functions (a concentration-response function) for selected causes of death., Results: In models stratified by age, sex, airshed, and population centre size, and adjusted for individual and neighbourhood socioeconomic variables, HR estimates for non-accidental mortality were HR = 1.18 (95% CI: 1.15-1.21) per 10μg/m 3 increase in concentration. We observed higher HRs for cardiovascular disease (HR=1.25; 95% CI: 1.19-1.31), cardio-metabolic disease (HR = 1.27; 95% CI: 1.21-1.33), ischemic heart disease (HR = 1.36; 95% CI: 1.28-1.44) and chronic obstructive pulmonary disease (COPD) mortality (HR = 1.24; 95% CI: 1.11-1.39) compared to HR for all non-accidental causes of death. For non-accidental, cardio-metabolic, ischemic heart disease, respiratory and COPD mortality, the shape of the concentration-response curve was supra-linear, with larger differences in relative risk for lower concentrations. For both pneumonia and lung cancer, there was some suggestion that the curves were sub-linear., Conclusions: Associations between ambient concentrations of fine particulate matter and several causes of death were non-linear for each cause of death examined., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Recent collection data indicate that at least four potential malaria vectors occupy more widespread distributions within the Andean highlands than in the past. Since habitat elimination is an important aspect of malaria control, it is vital to characterize larval habitats for Anopheles species within both lowland and highland sites. To that end, 276 sites within Ecuador were surveyed between 2008 and 2010. Characteristics of Anopheles-present sites for four species were compared to Anopheles-absent sites within the same geographical range and also to Anopheles-absent sites within a highland range representing potential future habitats. Thermochron iButtons(©) were used to describe the daily temperature variation within a subset of potential habitats. Anopheles albimanus (W.) was positively associated with permanent habitats, sand substrates, floating algae (cyanobacterial mats), and warmer temperatures in both comparisons. Anopheles pseudopunctipennis (T.) was associated with floating algae (cyanobacterial mats), warmer temperatures, and higher water clarity in both comparisons. Anopheles punctimacula (D.&K.) was negatively associated with floating algae and positively associated with dissolved oxygen in both comparisons. Anopheles oswaldoi s.l. (P.) was not significantly associated with any parameters more often than expected given larval-absent sites. The results indicate that minimum water temperatures might limit the upper altitudinal distribution of An. albimanus (18.7° C) and An. pseudopunctipennis (16.0° C)., (© 2012 The Society for Vector Ecology.)

Larval habitat for three highland Anopheles species: Anopheles albimanus Wiedemann, Anopheles pseudopunctipennis Theobald, and Anopheles punctimacula Dyar and Knab was related to human land uses, rivers, roads, and remotely sensed land cover classifications in the western Ecuadorian Andes. Of the five commonly observed human land uses, cattle pasture (n = 30) provided potentially suitable habitat for A. punctimacula and A. albimanus in less than 14% of sites, and was related in a principal components analysis (PCA) to the presence of macrophyte vegetation, greater surface area, clarity, and algae cover. Empty lots (n = 30) were related in the PCA to incident sunlight and provided potential habitat for A. pseudopunctipennis and A. albimanus in less than 14% of sites. The other land uses surveyed (banana, sugarcane, and mixed tree plantations; n = 28, 21, 25, respectively) provided very little standing water that could potentially be used for larval habitat. River edges and eddies (n = 41) were associated with greater clarity, depth, temperature, and algae cover, which provide potentially suitable habitat for A. albimanus in 58% of sites and A. pseudopunctipennis in 29% of sites. Road-associated water bodies (n = 38) provided potential habitat for A. punctimacula in 44% of sites and A. albimanus in 26% of sites surveyed. Species collection localities were compared to land cover classifications using Geographic Information Systems software. All three mosquito species were associated more often with the category "closed/open broadleaved evergreen and/or semi-deciduous forests" than expected (P ≤ 0.01 in all cases), given such a habitat's abundance. This study provides evidence that specific human land uses create habitat for potential malaria vectors in highland regions of the Andes.

Background: Several recent climate change reviews have stressed the possibility of some malaria vectors occupying regions of higher altitudes than previously recorded. Indeed, highland malaria has been observed in several African nations, possibly attributable to changes in land use, vector control and local climate. This study attempts to expand the current knowledge of the distribution of common Anopheles species in Ecuador, with particular attention to highland regions (> 500 m) of the Andes., Methods: Extensive field collections of larvae were undertaken in 2008, 2009 and 2010 throughout all regions of Ecuador (except the lower-altitude Amazonian plain) and compared to historical distribution maps reproduced from the 1940s. Larvae were identified using both a morphological key and sequencing of the 800 bp region of the CO1 mitochondrial gene. In addition, spatial statistics (Getis-Ord Hotspot Analysis: Gi*) were used to determine high and low-density clusters of each species in Ecuador., Results: Distributions have been updated for five species of Anopheles in Ecuador: Anopheles albimanus, Anopheles pseudopunctipennis, Anopheles punctimacula, Anopheles eiseni and Anopheles oswaldoi s.l.. Historical maps indicate that An. pseudopunctipennis used to be widespread in highland Andean valleys, while other species were completely restricted to lowland areas. By comparison, updated maps for the other four collected species show higher maximum elevations and/or more widespread distributions in highland regions than previously recorded. Gi* analysis determined some highland hot spots for An. albimanus, but only cold spots for all other species., Conclusions: This study documents the establishment of multiple anopheline species in high altitude regions of Ecuador, often in areas where malaria eradication programs are not focused.

To control malaria effectively, it is essential to understand the current knowledge, beliefs, concerns, land management practices, and mosquito bite protection methods in use by citizens. This study presents a comparative, quantitative, interview-based study of land owners and/or managers (n = 262) in the Ecuadorian lowlands (presently considered malarious) (n = 131) and highlands (potentially malarious in the future) (n = 131). Although respondents had a strong understanding of where the disease occurs in their own country and of the basic relationship among standing water, mosquitoes, and malaria, about half of respondents in potential risk areas denied the current possibility of malaria infection on their own property. As well, about half of respondents with potential anopheline larval habitat did not report its presence, likely due to a highly specific definition of suitable mosquito habitat. Most respondents who are considered at risk of malaria currently use at least one type of mosquito bite prevention, most commonly bed nets.