Exposure to tobacco smoke during pregnancy has been associated with a series of adverse reproductive outcomes; however, the underlying molecular mechanisms are not well-established. We conducted an untargeted metabolome-wide association study to identify the metabolic perturbations and molecular mechanisms underlying the association between cotinine, a widely used biomarker of tobacco exposure, and adverse birth outcomes. We collected early and late pregnancy urine samples for cotinine measurement and serum samples for high-resolution metabolomics (HRM) profiling from 105 pregnant women from the Atlanta African American Maternal-Child cohort (2014–2016). Maternal metabolome perturbations mediating prenatal tobacco smoke exposure and adverse birth outcomes were assessed by an untargeted HRM workflow using generalized linear models, followed by pathway enrichment analysis and chemical annotation, with a meet-in-the-middle approach. The median maternal urinary cotinine concentrations were 5.93 μg/g creatinine and 3.69 μg/g creatinine in early and late pregnancy, respectively. In total, 16,481 and 13,043 metabolic features were identified in serum samples at each visit from positive and negative electrospray ionization modes, respectively. Twelve metabolic pathways were found to be associated with both cotinine concentrations and adverse birth outcomes during early and late pregnancy, including tryptophan, histidine, urea cycle, arginine, and proline metabolism. We confirmed 47 metabolites associated with cotinine levels, preterm birth, and shorter gestational age, including glutamate, serine, choline, and taurine, which are closely involved in endogenous inflammation, vascular reactivity, and lipid peroxidation processes. The metabolic perturbations associated with cotinine levels were related to inflammation, oxidative stress, placental vascularization, and insulin action, which could contribute to shorter gestations. The findings will support the further understanding of potential internal responses in association with tobacco smoke exposures, especially among African American women who are disproportionately exposed to high tobacco smoke and experience higher rates of adverse birth outcomes.

The B-type cyclin gene, CycB2, serves as a negative regulator of glandular trichome initiation. Through targeted knockout of NtCycB2 in Nicotiana tabacum cv. K326 using the CRISPR/Cas9 system, we created a variety, HK326, which exhibits significantly increased density and larger glandular heads of long glandular trichomes. Under Cd-stress, HK326 exhibited enhanced Cd tolerance, as demonstrated by a robust root system, strengthened cell membrane stability, and higher photosynthetic parameters. HK326 exhibited enhanced Cd-stress tolerance due to a strong excretion capacity of long glandular trichomes by forming calcium oxalate crystals. Cd mainly accumulated in tobacco shoots rather than remained in roots. Specifically, Cd levels of the HK326 shoot surface were nearly two-fold of those of K326, resulting in less Cd internally in the roots and shoots. Gene expression patterns revealed 11 Cd transporter genes that were upregulated after Cd-stress in shoots, roots, and trichomes. Among them, the NtHMA2 gene encoding heavy metal ATPases and involved in the transport of divalent heavy metal cations was expressed consistently and significantly higher in HK326 than K326, both before and after Cd-stress. NtHMA2 expression was strong in trichomes, moderate in shoots, while weak in roots. The results indicate that NtHMA2 may be involved in Cd excretion from glandular trichomes. Our findings suggest HK326 may be an appropriate candidate plant for Cd-stress tolerance.

Nicotine (Nic) exposed to the environment which comes from tobacco products is the main addictive agent and specific classes of hazardous compound that merit concern. In this study, we have established a fast and reliable method to achieve specific detection of Nic in natural nicotiana tabacum within 30 s through a miniaturized platform based on screen printed gold electrode (SPE). A simple electrochemical pretreatment mean was employed on gold surface that led to the exposure of Au (111) facet and a convenient sample pretreatment method was adopted to realize the extraction of Nic in tobacco. The present electrochemical sensor exhibits an ample range of sensing from 10 μg/g to 200 μg/g, which is able to compliance with tobacco industry testing standards of actual samples. Over 60 sampling points from different origins in China or other countries were performed with direct analysis using this method and satisfactory results have been obtained. The proposed approach was demonstrated to be a very promising platform for significantly improving analytical efficiency in laboratories as well as for monitoring the source reduction control of Nic in the environment.

Tobacco is the most widespread non-food crop in the world. In Brazil, tobacco cultivation is one of the main commodities of the southern region. However, its production is associated with environmental impacts and risks to human health, which have yet to be quantified. This paper uses midpoint and endpoint life cycle assessment (LCA) to analyze the potential environmental damage and human health risk associated with agricultural production of conventional Virginia (CV), organic Virginia (OV), and Burley (BU) tobacco varieties. Organic tobacco production substitutes synthetic fertilizers and pesticides with organic compounds in the cropping stage. The results show that for one ton of dried tobacco, BU, CV, and OV emit 1,610, 1,426, and 1,091 kg CO₂ eq, respectively. For organic production, greater impacts are linked to the land use (LU) impact category. The endpoint results showed that OV production resulted in a higher potential for human and environmental damage than BU and CV. The drying of green OV and CV tobacco requires the burning of firewood, which emits high levels of particulate matter and is associated with human health (HH) damage. Overall, the HH damage category accounts for 68%, 82%, and 78% of the total score points associated with the production of BU, CV, and OV.

Air pollution has been identified as a major cause of environmental and human health damage. O₃ is an oxidative pollutant that causes leaf symptoms in sensitive plants. This study aims to adjust a multilinear model for the monitoring of O₃ in subtropical climatic conditions by associating O₃ concentrations with measurements of morphological leaf traits in tobacco plants and different environmental variables. The plants were distributed into five areas (residential, urban or industrial) in the southern region of Brazil and exposed during 14 periods, of 14 days each, during the years of 2014 and 2015. The environmental variables and leaf traits during the exposure periods were described by mean, median, standard deviation and minimum and maximum values. Spearman correlation and multiple linear regression analyses were applied on data from exposure periods. Leaf injury index, leaf area, leaf dry mass, temperature, relative humidity, global solar radiation and accumulated rainfall were used in the regression analyses to select the best models for predicting O₃ concentrations. Leaf injury characteristically caused by O₃ was verified in all areas and periods of plant exposure. Higher values of leaf injury (24.5% and 27.7%) were registered in the 13th and 12th exposure periods during spring and in areas influenced by urban and industrial clutches. The VPD, temperature, global solar radiation and O₃ were correlated to leaf injury. Environmental variables [leaf area, leaf dry mass, global solar radiation and accumulated rainfall] and primarily the VPD were fundamental to improve the adjustments done in the bioindicator model (R² ≥ 0.73). Our research shows that biomonitoring employing the tobacco “Bel-W3” can be improved by measuring morphological leaf traits and meteorological parameters. Additionally, O₃ fumigation experiment should be performed with biomonitoring as conducted in this study, which are useful in understanding the role of other environmental factors.

Smoking activities were recognized as a main risk factor for population. Indeed, mainstream smoke aerosol is directly inhaled by smokers then delivering harmful compounds in the deepest regions of the lung. In order to reduce the potential risk of smoking, different nicotine delivery products have been recently developed. The latest device released is an electrically heated tobacco system (iQOS®, Philip Morris) which is able to warm the tobacco with no combustion. In the present paper a dimensional and volatility characterization of iQOS-generated particles was performed through particle number concentration and distribution measurements in the mainstream aerosol. The experimental analysis was carried out through a condensation particle counter, a fast mobility particle sizer and a thermo-dilution sampling system allowing aerosol samplings at different temperatures. Estimates of the particle surface area dose received by smokers were also carried out on the basis of measured data and typical smoking patterns.The particle number concentrations in the mainstream aerosols resulted lower than 1 × 108 part. cm−3 with particle number distribution modes of about 100 nm. Nonetheless, the volatility analysis showed the high amount of volatile fraction of iQOS-generated particles, indeed, samplings performed at 300 °C confirmed a significant particle shrinking phenomena (modes of about 20 nm). Anyway, the particle number concentration does not statistically decrease at higher sampling temperatures, then showing that a non-volatile fraction is always presents in the emitted particles. The dose received by smokers in terms of non-volatile amount of particle surface area was equal to 1–2 mm2 per puff, i.e. up to 4-fold larger than that received by electronic cigarette vapers.

Congenital heart defects (CHDs) are a major cause of death in infancy and childhood. Major risk factors for most CHDs, particularly those resulting from the combination of environmental exposures with social determinants and behaviors, are still unknown. This study evaluated the main effect of maternal environmental tobacco smoke (ETS), and its interaction with social-demographics and environmental factors on CHDs in China. A population-based, matched case-control study of 9452 live-born infants and stillborn fetuses was conducted using the Guangdong Registry of Congenital Heart Disease data (2004–2014). The CHDs were evaluated by obstetrician, pediatrician, or cardiologist, and confirmed by cardia tomography/catheterization. Controls were randomly chosen from singleton newborns without any malformation, born in the same hospital as the cases and 1:1 matched by infant sex, time of conception, and parental residence (same city and town to ensure sufficient geographical distribution for analyses). Face-to-face interviews were conducted to collect information on demographics, behavior patterns, maternal disease/medication, and environmental exposures. Conditional logistic regression was used to estimate odds ratios and 95% confidence intervals of ETS exposure on CHDs while controlling for all risk factors. Interactive effects were evaluated using a multivariate delta method for maternal demographics, behavior, and environmental exposures on the ETS-CHD relationship. Mothers exposed to ETS during the first trimester of pregnancy were more likely to have infants with CHD than mothers who did not (aOR = 1.44, 95% CI 1.25–1.66). We also observed a significant dose-response relationship when mothers were exposed to ETS and an increasing number of risk factors and CHDs. There were greater than additive interactions for maternal ETS and migrant status, low household income and paternal alcohol consumption on CHDs. Maternal low education also modified the ETS-CHD association on the multiplicative scale. These findings may help to identify high-risk populations for CHD, providing an opportunity for targeted preventive interventions.

We tested seven contemporary agrochemicals as potential plant protectants against ozone phytotoxicity. In nine experiments, Bel-W3 tobacco plants were experienced weekly exposures to a) 80 nmol mol−1 of ozone-enriched or ozone-free air in controlled environment chambers, b) an urban air polluted area, and c) an agricultural-remote area. Ozone caused severe leaf injury, reduced chlorophylls' and total carotenoids' content, and negatively affected photosynthesis and stomatal conductance. Penconazole, (35% ± 8) hexaconazole (28% ± 5) and kresoxim-methyl (28% ± 15) showed higher plants’ protection (expressed as percentage; mean ± s.e.) against ozone, although the latter exhibited a high variability. Azoxystrobin (21% ± 15) showed lower protection efficacy and Benomyl (15% ± 9) even lower. Trifloxystrobin (7% ± 11) did not protect the plants at all. Acibenzolar-S-methyl + metalaxyl-M (Bion MX) (−6% ± 17) exhibited the higher variability and contrasting results: in some experiments it showed some protection while in others it intensified the ozone injury by causing phytotoxic symptoms on leaves, even in control plants.

Arabidopsis MRPs/ABCCs have been shown to remove various organic and inorganic substrates from the cytosol to other subcellular compartments. Here we first demonstrate that heterologous expression of AtMRP7 in tobacco (Nicotiana tabacum var. Xanthi) modifies cadmium accumulation, distribution and tolerance. Arabidopsis MRP7 was localized both in the tonoplast and in the plasma membrane when expressed in tobacco. Its overexpression increased tobacco Cd-tolerance and resulted in enhanced cadmium concentration in leaf vacuoles, indicating more efficient detoxification by means of vacuolar storage. Heterologous AtMRP7 expression also led to more efficient retention of Cd in roots, suggesting a contribution to the control of cadmium root-to-shoot translocation. The results underscore the use of AtMRP7 in plant genetic engineering to modify the heavy-metal accumulation pattern for a broad range of applications.

Genotoxicity of urban air has been analysed almost exclusively in airborne particulates. We monitored the genotoxic effects of airborne pollutants in the urban air of Perugia (Central Italy). Two plant bioindicators with different genetic endpoints were used: micronuclei in meiotic pollen mother cells using Tradescantia-micronucleus bioassay (Trad-MCN) and DNA damage in nuclei of Nicotiana tabacum leaves using comet assay (Nicotiana-comet). Buds of Tradescantia clone # 4430 and young N. tabacum cv. Xanthi plants were exposed for 24 h at three sites with different pollution levels. One control site (indoor control) was also used. The two bioassays showed different sensitivities toward urban pollutants: Trad-MCN assay was the most sensitive, but DNA damage in N. tabacum showed a better correlation with the pollutant concentrations. In situ biomonitoring of airborne genotoxins using higher plants combined with chemical analysis is thus recommended for characterizing genotoxicity of urban air. Plant bioassays used to explore in situ the correlation between air pollution and genotoxicity.