As the underlying mechanisms of the adverse effects of cold spells on cardiac events are not well understood, we explored the effects of cold spells on plasma viscosity, a blood parameter linked to cardiovascular disease. This cross-sectional study involved 3622 participants from the KORA S1 Study (1984–1985), performed in Augsburg, Germany. Exposure data was obtained from the Bavarian State Office for the Environment. Cold spells were defined as two or more consecutive days with daily mean temperatures below the 3ʳᵈ, 5ᵗʰ, or 10ᵗʰ percentile of the distribution. The effects of cold spells on plasma viscosity were explored by generalized additive models with distributed lag nonlinear models (DLNM). We estimated cumulative effects at lags 0–1, 0–6, 0–13, 0–20, and 0–27 days separately. Cold spells (mean temperature <3ʳᵈ, <5ᵗʰ or <10ᵗʰ percentile) were significantly associated with an increase in plasma viscosity with a lag of 0–1 days [%change of geometric mean (95% confidence interval): 1.35 (0.06–2.68), 1.35 (0.06–2.68), and 2.49 (0.34–4.69), respectively], and a lag of 0–27 days [18.81 (8.97–29.54), 17.85 (8.29–28.25), and 7.41 (3.35–11.0), respectively]. For the analysis with mean temperature <3ʳᵈ or 10ᵗʰ percentile, we also observed significant associations at lag 0–20 days [8.34 (0.43–16.88), and 4.96 (1.68, 8.35), respectively]. We found that cold spells had significant immediate and longer lagged effects on plasma viscosity. This finding supports the complex interplay of multiple mechanisms of cold on adverse cardiac events and enriches the knowledge about how cold exposure acts on the human body.

The association between temperature and mortality has been widely reported. However, it remains largely unclear whether inflammation-related diseases, caused by excessive or inappropriate inflammatory reaction, may be affected by ambient temperature, particularly in low-income areas.To explore the association between ambient temperature and clinical visits for inflammation-related diseases in rural villages in the Ningxia Hui Autonomous Region, China, during 2012─2015.Daily data on inflammation-related diseases and weather conditions were collected from 258 villages in Haiyuan (161 villages) and Yanchi (97 villages) counties during 2012─2015. A Quasi-Poisson regression with distributed lag non-linear model was used to examine the association between temperature and clinical visits for inflammation-related diseases. Stratified analyses were performed by types of diseases including arthritis, gastroenteritis, and gynecological inflammations.During the study period, there were 724,788 and 288,965 clinical visits for inflammation-related diseases in Haiyuan and Yanchi, respectively. Both exposure to low (RR: 2.045, 95% CI: 1.690, 2.474) and high temperatures (RR: 1.244, 95% CI: 1.107, 1.399) were associated with increased risk of total inflammation-related visits in Haiyuan county. Low temperatures were associated with increased risks of all types of inflammation-related diseases in Yanchi county (RR: 4.344, 95% CI: 2.887, 6.535), while high temperatures only affected gastroenteritis (RR: 1.274, 95% CI: 1.040, 1.561). Moderate temperatures explained approximately 26% and 33% of clinical visits due to inflammation-related diseases in Haiyuan and Yanchi, respectively, with the burden attributable to cold exposure higher than hot exposure. The reference temperature values ranged from 17 to 19 in Haiyuan, and 12 to 14 in Yanchi for all types of clinical visits.Our findings add additional evidence for the adverse effect of suboptimal ambient temperature and provide useful information for public health programs targeting people living in rural villages.

The purpose of this study is to verify the hypothesis that chronic obstructive pulmonary disease (COPD) model rat is more susceptible to cold stress and fine particulate matter (PM2.5) exposure than the healthy rat, and explore the related mechanism. COPD rat model, established with cigarette smoke and lipopolysaccharide intratracheal instillation, were exposed to cold stress (0 °C) and PM2.5 (0, 3.2, 12.8 mg/ml). After that, the levels of superoxide dismutase, inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-α), monocyte chemotactic protein 1 (MCP-1) and angiotensin Ⅱ (Ang-Ⅱ) in lung were measured, as well as the expression levels of lung 8-hydroxy-2-deoxyguanosine (8-OHdG), nuclear factor kappa B (NF-κB), heme-oxygenase-1 (HO-1) and nuclear factor erythroid-2-related factor 2 (Nrf2). There were significant positive relationships between PM2.5 and lung level of iNOS, TNF-α, MCP-1 and Ang-Ⅱ, lung function and pathologic damage in COPD rats. The HO-1, NF-κB and 8-OHdG were found highly expressed in COPD rat lung, particularly at the higher PM2.5 dose of cold stress groups, while Nrf2 was found declined. Thus, COPD rats may be more susceptible to cold stress and PM2.5 exposure. Cold stress may aggravate PM2.5-induced toxic effects in the lung of COPD rats through increasing Ang-Ⅱ/NF-κB signaling pathway and suppressing Nrf2 signaling pathway.

Previous studies have suggested that ambient temperature is associated with the mortality and morbidity of myocardial infarction (MI) although consistency among these investigations is lacking. We performed a meta-analysis to investigate the relationship between ambient temperature and MI. The PubMed, Web of Science, and China National Knowledge Infrastructure databases were searched back to August 31, 2017. The pooled estimates for different temperature exposures were calculated using a random-effects model. The Cochran's Q test and coefficient of inconsistency (I2) were used to evaluate heterogeneity, and the Egger's test was used to assess publication bias. The exposure-response relationship of temperature-MI mortality or hospitalization was modeled using random-effects meta-regression. A total of 30 papers were included in the review, and 23 studies were included in the meta-analysis. The pooled estimates for the relationship between temperature and the relative risk of MI hospitalization was 1.016 (95% confidence interval [CI]: 1.004–1.028) for a 1 °C increase and 1.014 (95% CI: 1.004–1.024) for a 1 °C decrease. The pooled estimate of MI mortality was 1.639 (95% CI: 1.087–2.470) for a heat wave. The heterogeneity was significant for heat exposure, cold exposure, and heat wave exposure. The Egger's test revealed potential publication bias for cold exposure and heat exposure, whereas there was no publication bias for heat wave exposure. An increase in latitude was associated with a decreased risk of MI hospitalization due to cold exposure. The association of heat exposure and heat wave were immediate, and the association of cold exposure were delayed. Consequently, cold exposure, heat exposure, and exposure to heat waves were associated with an increased risk of MI. Further research studies are required to understand the relationship between temperature and MI in different climate areas and extreme weather conditions.

Non-optimum ambient temperature has been associated with a variety of health outcomes in the elderly population. However, few studies have examined its adverse effects on neurocognitive function. In this study, we explored the temperature-cognition association in elderly women. We investigated 777 elderly women from the German SALIA cohort during the 2007–2010 follow-up. Cognitive function was evaluated using the CERAD-Plus test battery. Modelled data on daily weather conditions were assigned to the residential addresses. The temperature-cognition association over lag 0–10 days was estimated using multivariable regression with distributed lag non-linear model. The daily mean temperature ranged between −6.7 and 26.0 °C during the study period for the 777 participants. We observed an inverse U-shaped association in elderly women, with the optimum temperature (15.3 °C) located at the 68th percentile of the temperature range. The average z-score of global cognitive function declined by −0.31 (95%CI: 0.73, 0.11) for extreme cold (the 2.5th percentile of temperature range) and −0.92 (95%CI: 1.50, −0.33) for extreme heat (the 97.5th percentile of temperature range), in comparison to the optimum temperature. Episodic memory was more sensitive to heat exposure, while semantic memory and executive function were the two cognitive domains sensitive to cold exposure. Individuals living in an urban area and those with a low educational level were particularly sensitive to extreme heat. In summary, non-optimum temperature was inversely associated with cognitive function in elderly women, with the effect size for heat exposure particularly substantial. The strength of association varied by cognitive domains and individual characteristics.

The increase in population in urban areas has increased the demand for housing. In cities that could not adapt to the population increase, the attempt to fit more houses in a unit area has emerged. This situation caused the application of created designs ignoring the natural and microclimate data of the cities. Since Erzurum is located on the high plain surrounded by mountains, it is one of the coldest cities in Turkey with its long-term annual mean temperature of 5.7 °C. The aim of this research is to reveal the effects of the urban morphology on thermal comfort and its relationship with air pollution in Erzurum. Steps of the research methodology can be summarized as determination of measurement areas, physiologically equivalent temperature (PET) analysis, air pollution analysis, and mapping. The city center is located at an altitude of 1850 m from the sea level, and the open rural area has the lowest altitude of 1650 m from the sea level with respect to the surrounding mountainous terrain. The microclimate data of the meteorological stations in the three study areas and government monitoring station and air pollution data have been recorded hourly in 2018. The recorded data was analyzed with the RayMan pro 2.1 model, which is a widely used simple index PET for obtaining outdoor thermal comfort. According to the research results, the highest PET value of Erzurum was obtained in the city center as 11.4 °C and then the urban transformation district as 6.3 °C, and the lowest PET was obtained from the open rural area as 4.5 °C. In the areas that have low PET values and cold stress issues, it was observed that the air pollution data are low. The city center was detected to have the highest air pollution parameters. It was determined that urban morphology, air pollution, and thermal comfort had significant correlations.

Exposure to suboptimal ambient temperature during pregnancy has been reported as a potential teratogen of fetal development. However, limited animal evidence is available regarding the impact of extreme temperatures on maternal pregnancy and the subsequent adverse pregnancy outcomes. Our objective in this study is to investigate the relationship between temperature and maternal stress during pregnancy in mice. This study used the Naval Medical Research Institute (NMRI) mice during the second and third pregnant weeks with the gestational day (GD) (GD 6.5–14.5 and GD 14.5–17.5). Mice were exposed to suboptimal ambient temperature (1 °C, 5 °C, 10 °C, 15 °C, 40 °C, 42 °C, 44 °C, 46 °C, and 48 °C for the experimental group and 23 °C for the control group) 1 h per day, 7 days a weekin each trimester. Measurements of placental development (placental weight [PW] and placental diameter [PD]) and fetal growth (fetal weight [FW] and crown-to-rump length [CRL]) between experimental and control groups were compared using analysis of variance (ANOVA). Data on the occurrence of preterm birth (PTB) and abnormalities were also collected. The results showed that exposure to both cold and heat stress in the second and third weeks of pregnancy caused significant decreases in measurements of placental development (PW and PD) and fetal growth (FW and CRL). For all temperature exposures, 15 °C was identified as the optimal temperature in the development of the embryo. Most PTB occurrences were observed in high-temperature stress groups, with the highest PTB number seen in the exposure group at 48 °C, whereas PTB occurred only at 1 °C among cold stress groups. In the selected exposure experiments, an approximate U-shaped relation was observed between temperature and number of abnormality occurrence. The highest percentage of these anomalies occurred at temperatures of 1 °C and 48 °C, while no abnormalities were observed at 15 °C and in the control group. Our findings strengthened the evidence that exposure to suboptimal ambient temperatures may trigger adverse pregnancy outcomes and worsen embryo and fetal development in mice.

Previous studies have indicated that capsaicin-rich diet and cold weather have shown strong association with tumor incidence. Thus, we investigated the effects of capsaicin and cold exposure in 1,2-dimethylhydrazine (DMH)-induced colorectal cancer as well as the mechanisms underlying capsaicin and cold-induced CRC. Rats were randomly divided into four groups and received cold still water and capsaicin via intragastric gavage until the end of the experiment. The rat’s body weight, thymus weight, and food intakes were assessed. Global levels of histone H3K9, H3K18, H3K27, and H4K16 acetylation and histone deacetylase (HDACs) in colon mucosa were assessed by western blot. Expression levels of Toll-like receptors 2 (TLR2) and Toll-like receptors 4 (TLR4) were measured by western blot and reverse-transcriptase quantitative polymerase chain reaction (qPCR). We found that cold and low-dose capsaicin increased tumor numbers and multiplicity, although there were no differences in tumor incidence. Additionally, rat exposure to cold water and capsaicin display further higher levels of histone H3 lysine 9 (H3K9AC), histone H3 lysine 18 (H3K18AC), histone H3 lysine 27 (H3K27AC), and HDACs compared with the DMH and normal rats. In contrast, a considerable decrease of histone H4 lysine 16 (H4K16AC) was detected in the colon mucosa. Cold and low-dose capsaicin exposure groups were also increased TLR2 and TLR4 protein levels and mRNA levels. These results suggest that chronic cold exposure and capsaicin at a low-dose intervention exacerbate ectopic expression of global histone acetylation and TLR level, which are crucial mechanisms responsible for the progression of colorectal cancer in rats.

MicroRNAs (miRNAs) are one of the most critical epigenetic regulators of gene expression which modulate a spectrum of development and defence response processes in plants. Chromium (Cr) contamination in rice imposes a serious concern to human health as rice is used as staple food throughout the world. Although several studies have established the differential response of miRNAs in rice during heavy metal (arsenic, cadmium) and heat or cold stress, no report is available about the response of miRNAs during Cr stress. In the present study, we identified 512 and 568 known miRNAs from Cr treated and untreated samples, respectively. Expression analysis revealed that 13 conserved miRNAs (miR156, miR159, miR160, miR166, miR169, miR171, miR396, miR397, miR408, miR444, miR1883, miR2877, miR5072) depicted preferential up- or down-regulation (> 4-fold change; P value < 0.05). Target gene prediction of differentially expressed miRNAs and their functional annotation suggested the important role of miRNAs in defence and detoxification of Cr though ATP-binding cassette transporters (ABC transporters), transcription factors, heat shock proteins, auxin response, and metal ion transport. Real-time PCR analysis validated the differential expression of selected miRNAs and their putative target genes. In conclusion, our study identifies and predicts miRNA-mediated regulation of signalling pathway in rice during Cr stress.

Persistent environmental pollutants are a growing problem around the world. The effective control of the pollutants is of great significance for human health. Some microbes, especially Arthrobacter, can degrade pollutants into nontoxic substances in various ways. Here, we review the biological properties of Arthrobacter adapting to a variety of environmental stresses, including starvation, hypertonic and hypotonic condition, oxidative stress, heavy metal stress, and low-temperature stress. Furthermore, we categorized the Arthrobacter species that can degrade triazines, organophosphorus, alkaloids, benzene, and its derivatives. Metabolic pathways behind the various biodegradation processes are further discussed. This review will be a helpful reference for comprehensive utilization of Arthrobacter species to tackle environmental pollutants.