Sentences with phrase «exposure to cigarette smoke in»

The role of exposure to cigarette smoke in bladder cancer risk in dogs requires more study, but it would be best to limit exposure to smoke as it can cause other disease in dogs too.

Not exact matches

Free Radical Protection: The high levels of antioxidants in Cacao Powder can help protect the body from free radicals such as cigarette smoke, sun exposure, and pollution which may lead to cancer and cardiovascular disease.

Despite the high cadmium content in cigarette smoke, there seems to be little exposure to cadmium from passive smoking.

Studies show that a baby's risk of SIDS rises with each additional smoker in the household, with the number of cigarettes smoked around her each day, and with the length of her exposure to cigarette smoke.

Exposure to environmental tobacco smoke was recorded as the number of hours (during the previous 24 hours) spent in a room with someone smoking cigarettes.

Relation of infant feeding practices, cigarette smoke exposure, and group child care to the onset and duration of otitis media with effusion in the first two years of life.

Information on socioeconomic background, maternal diseases and obstetric history, parity, gender, fetal exposure to alcohol (at least 2 drinks a week during the entire pregnancy) and cigarette smoking (at least 1 cigarette a day during the last trimester), type and duration of breastfeeding, and maternal intelligence (Raven Progressive Matrices) was obtained through questionnaires administered in person after delivery and at 13 months.

In animal models, exposure to cigarette smoke or nicotine during fetal development alters the expression of the nicotinic acetylcholine receptor in areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDIn animal models, exposure to cigarette smoke or nicotine during fetal development alters the expression of the nicotinic acetylcholine receptor in areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin areas of the brainstem important for autonomic function, 28 alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDIn human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDin autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDS.

Recent studies have explored how prenatal exposure to cigarette smoke may result in an increased risk of SIDS.

Chronic cigarette smoke exposure, as noted in many human cancers, tends to block these cell maturation genes from properly turning on, says Baylin.

The amount of nicotine in the rats» blood after exposure to cigarette smoke was similar to the amount in blood after humans have smoked one cigarette, confirming that the exposure conditions were relevant to the real world.

One study of e-cigarettes was conducted to resemble a smoky bar: the researchers found that markers of nicotine in nonsmokers who sat nearby was similar for both cigarette smoke and e-cigarette aerosol exposure.

«We know that exposure to smoking cues such as visual depictions of cigarettes, ashtrays, matches, lighters, and smoke heightens smokers» urge to smoke a cigarette, and decreases former smokers» confidence in their ability to refrain from smoking a cigarette,» said Dr. Maloney.

Conklin also said that chronic exposures to smokeless tobacco extracts, mainstream cigarette smoke, acrolein, or e-cigarette aerosol enhanced atherosclerotic lesion formation in a mouse model of atherosclerosis.

As lead author Laura Rupprecht said, «The findings are important in the context of potential product standards requiring very low nicotine levels in cigarettes, as they indicate that low nicotine levels may still reduce body weight, possibly motivating continued use and maintaining exposure to harmful chemicals in cigarette smoke.»

DCEG investigators are also working to identify novel molecular and genomic signatures in tumors that are linked to germline genetic variants and environmental exposures, such as cigarette smoking and ionizing radiation.

Owing to the large effect of tobacco smoke at low doses, exposure to second - hand smoke in the reference group (never smokers) might lead to underestimation of the relative risk for one and 20 cigarettes per day and consequently dilute the percentage effect of one compared with 20 cigarettes per day.

Three recent experimental studies focused on low consumption / exposure.949596 In one study, 29 smokers each consumed a single cigarette, immediately after which they had a significant decrease in blood vessel output power and significant increase in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.In one study, 29 smokers each consumed a single cigarette, immediately after which they had a significant decrease in blood vessel output power and significant increase in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.in blood vessel output power and significant increase in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.in blood vessel ageing level and remaining blood volume 25 minutes later, as markers of atherosclerosis.94 In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.In another study, human coronary artery endothelial cells were exposed to the smoke equivalent to one cigarette, which led to activation of oxidant stress sensing transcription factor NFR2 and up - regulation of cytochrome p450, considered to have a role in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.in the development of heart disease.95 These effects were not seen when heart cells were exposed to the vapour from one e - cigarette.95 A study exposed adult mice to low intensity tobacco smoke (two cigarettes) for one to two months and found adverse histopathological effects on brain cells.96

[12] Cancers that respond the most favorably to checkpoint inhibitors include non — small - cell lung cancer, largely caused by chronic exposure to carcinogens in cigarette smoke, and melanoma, largely caused by exposure to ultraviolet light.

Both cigarette smoke and nicotine have been shown to inhibit pulmonary T cell responses, including secretion of IFNγ, and enhance susceptibility to virus infection [31, 33], which suggests that exposure to nicotine, such as in E-cigs, may exhibit immunosuppressive effects.

In conclusion, E-cig exposure results in immunomodulatory effects that are similar to those observed after exposure to cigarette smokIn conclusion, E-cig exposure results in immunomodulatory effects that are similar to those observed after exposure to cigarette smokin immunomodulatory effects that are similar to those observed after exposure to cigarette smoke.

«This study suggests that smokers who completely switch to e-cigarettes and stop smoking tobacco cigarettes may significantly reduce their exposure to many cancer - causing chemicals,» said lead author Maciej Goniewicz, an assistant professor of oncology at Roswell Park Cancer Institute in Buffalo, N.Y.

It processes literally everything that passes through our body, and it's safe to say that most of us probably have a chemical overload — toxins enter our body from numerous places in our environment (pollution, car fumes, cigarette smoke, sun exposure), food (additives, chemicals, artificial flavours, sweeteners, food colouring) and body care products (sodium lauryl sulfate, and too many others to name!)

It is thought to be useful in situations involving exposure to environmental toxins such as cigarette smoke or air pollution, heavy metals such as mercury, lead or arsenic in the blood.

Living together with a cigarette smoker increases the chance of dying from lung cancer and heart disease, and in children smoke exposure increase the severity of the intensity of asthma attacks and leads to in excess of 750,000 middle ear infections, as reported by the American Cancer Society.

The causes vary from exposure to poor quality air, pesticides in foods, and toxins from cigarette smoke.

According to Mark Sircus, in Transdermal Magnesium Therapy, a deficiency of magnesium increases free radical generation in the body and «causes glutathione loss, which is not affordable because glutathione helps to defend the body against damage from cigarette smoking, exposure to radiation, cancer chemotherapy, and toxins such as alcohol and just about everything else.»

Metallothionine is increased aggressively by exposure to the carcinogenic cadmium in cigarette smoke, probably contributing to the addictive properties of the nicotine, therein.

Exposure to cigarette smoke, environmental pollutants, and the UV light from the sun all decrease the amount of vitamin C in the skin.

There are, however, other factors that can increase the production of free radicals, and many of them go hand in hand with modern day life: unhealthy food, exposure to pesticides, herbicides, cleaning chemicals, and cigarette smoke, and physical and emotional stress.

Chronic exposure to inhaled irritants (including cigarette smoke) may be a cause of bronchitis in the dog.

Other causes include diets low in Vitamin A & E, excessive use of grooming perches, lack of exercise, and exposure to cigarette smoke.

The lining of the respiratory tract can be debilitated through exposure to cold temperatures; dust, cigarette smoke or other particles in the air; stressful situations like travel; and time spent in crowded conditions like those found in many animal shelters and boarding kennels.

There is a growing body of information suggesting that fetal exposures to maternal stress and parental cigarette smoking contribute to the expression of asthma in young children.

Moreover, this conspiracy, if proven, relates to matters of significance in Ontario — allegedly misleading the public and the government about the harmful effects of cigarettes and exposure to second hand smoke.»

When limited to 146 households with exposure to cigarette smokers over time (ie, participants who completed a 7 - month visit and had at least one smoker in the household at any time point), 69 % (101/146) reported being smoke - free antepartum.

Consider the deadly Stachybotrys mold, which when combined with exposure to cigarette smoke, can cause fatal bleeding in the lungs of babies under 12 months old.