Smoking enhances the expression of angiotensin‐converting enzyme 2 involved in the efficiency of severe acute respiratory syndrome coronavirus 2 infection

Suzuki, Rigel; Ono, Yuki; Noshita, Koji; Kim, Kwang Su; Ito, Hayato; Morioka, Yuhei; Tamura, Tomokazu; Okuzaki, Daisuke; Tagawa, Tetsuzo; Takenaka, Tomoyoshi; Yoshizumi, Tomoharu; Shimamura, Teppei; Iwami, Shingo; Fukuhara, Takasuke

doi:10.1111/1348-0421.13034

Cited by 5 publications

(8 citation statements)

References 35 publications

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“…inconclusive rather than evidence of no effect. There are several indicators that a real effect is plausible, including considerable mechanistic and epidemiological evidence that PM2.5 increases vulnerability to COVID-19 for a sustained amount of time (1)(2)(3)6,7). In addition, point estimates in our study were consistently positive across 12 separate models.…”

Section: Association Between Pm25 and Covid-19 Outcomessupporting

confidence: 53%

“…There is limited direct evidence on whether extreme but discrete PM2.5 exposures like a coalmine fire increase long-term vulnerability to COVID-19. However, circumstantial evidence suggests this may be the case, such as higher expression of ACE2 in current and former smokers than non-smokers (6,7). And in Mexico City, PM2.5 measurements from 2000-2018 were associated with COVID-19 deaths in 2020, even when adjusting for PM2.…”

Section: Introductionmentioning

confidence: 99%

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Long-term effects of extreme smoke exposure on COVID-19: A cohort study

Lane

Carroll

Borg

et al. 2023

Preprint

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In early 2014, the Hazelwood coalmine fire covered the regional Australian town of Morwell in smoke and ash for 45 days. One of the fire’s by-products, PM2.5, has been linked higher rates of COVID-19 infection to increased expression of the ACE2 receptor, which the COVID-19 virus uses to infect cells throughout the body. However, it is unclear whether the effect persists for years after exposure. In this study, we surveyed a cohort established prior to the pandemic to determine whether PM2.5from the coalmine fire increased long-term vulnerability to COVID-19 infection and severe disease.In late 2022, 612 members of the Hazelwood Health Study’s adult cohort, established in 2016/17, participated in a follow-up survey including standardised items to capture COVID-19 infections, hospitalisations, and vaccinations. Associations were evaluated in crude and adjusted logistic regression models, applying statistical weighting for survey response and multiple imputation to account for missing data, with sensitivity analyses to test the robustness of results.A total of 271 (44%) participants self-reported or met symptom criteria for at least one COVID-19 infection. All models found a positive association, with odds of infection increasing by between 4-21% for every standard deviation (12.3µg/m3) increase in mine fire-related PM2.5exposure. However, this was not statistically significant in any model. There were insufficient hospitalisations to examine severity (n=7; 1%).The findings were inconclusive in ruling out an effect of PM2.5exposure from coalmine fire on long-term vulnerability to COVID-19 infection. Given the positive association that was robust to modelling variations as well as evidence for a causal mechanism, it would be prudent to treat PM2.5from fire events as a risk factor for long-term COVID-19 vulnerability until more evidence accumulates.

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Section: Association Between Pm25 and Covid-19 Outcomessupporting

confidence: 53%

Section: Introductionmentioning

confidence: 99%

Long-term effects of extreme smoke exposure on COVID-19: A cohort study

Lane

Carroll

Borg

et al. 2023

Preprint

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“…In addition, there is considerable mechanistic and epidemiological evidence that PM 2.5 increases vulnerability to COVID-19, 1-3 which may be sustained for at least a year after exposure. 7,8 Yet there remain reasons to doubt such an effect. Associations were only sporadically significant, and only when using the symptom-identified COVID-19 outcome, which was vulnerable to misclassification (see below).…”

Section: Discussionmentioning

confidence: 99%

“…For instance, current and former smokers both exhibit higher expression of ACE2 than non-smokers. 7,8 And in Mexico City, PM 2.5 measurements from 2000 to 2018 were associated with COVID-19 deaths in 2020, even when adjusting for PM 2.5 exposures in 2019 and the weeks preceding infection. 9 Equivalent amounts of PM 2.5 from landscape fires may be more hazardous than ambient urban background sources, 10 meaning even short-term exposures could cause substantial long-term harm.…”

Section: Introductionmentioning

confidence: 98%

Long‐term effects of extreme smoke exposure on COVID‐19: A cohort study

Lane,

Carroll,

Borg

et al. 2023

Respirology

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BackgroundIn 2014, the Hazelwood coalmine fire shrouded the regional Australian town of Morwell in smoke and ash for 6 weeks. One of the fire's by‐products, PM2.5, is associated with an increased risk of COVID‐19 and severe disease. However, it is unclear whether the effect persisted for years after exposure. In this study, we surveyed a cohort established prior to the pandemic to determine whether PM2.5 from the coalmine fire increased long‐term vulnerability to COVID‐19 and severe disease.MethodsFrom August to December 2022, 612 members of the Hazelwood Health Study's adult cohort, established in 2016/17, participated in a follow‐up survey that included standardized items to capture COVID‐19 cases, as well as questions about hospitalization and vaccinations. Associations were evaluated in crude and adjusted logistic regression models.ResultsA total of 268 (44%) participants self‐reported or met symptom criteria for having had COVID‐19 at least once. All models found a positive association, with odds of COVID‐19 increasing by between 4% and 30% for a 10 μg/m3 increase in coalmine fire‐related PM2.5 exposure. However, the association was significant in only 2 of the 18 models. There were insufficient hospitalizations to examine severity (n = 7; 1%).ConclusionThe findings are inconclusive on the effect of coalmine fire‐related PM2.5 exposure on long‐term vulnerability to COVID‐19. Given the positive association that was robust to modelling variations as well as evidence for a causal mechanism, it would be prudent to treat PM2.5 from fire events as a long‐term risk factor until more evidence accumulates.

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“…The COVID-19 pandemic offers an important opportunity to examine how viral infections might aggravate PD-related neurodegeneration [ 82 ]. Table 1 summarizes the mechanisms underlying the aggravation of PD-related neurodegenerations due to SARS-CoV-2 [ 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 , 95 , 96 , 97 , 98 , 99 , 100 , 101 , 102 , 103 , 104 , 105 , 106 , 107 , 108 , 109 , 110 , 111 , 112 , 113 , 114 , 115 , 116 , 117 , 118 , 119 , 120 , 121 ] and Figure 3 summarizes the specific pathways involved in ACE2 dysregulation as a connecting link between COVID-19 and PD.…”

Section: Ace2 In Pd and Covid-19: Connecting The Dotsmentioning

confidence: 99%

Exploring the Role of ACE2 as a Connecting Link between COVID-19 and Parkinson’s Disease

Angelopoulou

Karlafti

Georgakopoulou

et al. 2023

Life

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Coronavirus disease 2019 (COVID-19) is frequently accompanied by neurological manifestations such as headache, delirium, and epileptic seizures, whereas ageusia and anosmia may appear before respiratory symptoms. Among the various neurological COVID-19-related comorbidities, Parkinson’s disease (PD) has gained increasing attention. Some cases of PD disease have been linked to COVID-19, and both motor and non-motor symptoms in Parkinson’s disease patients frequently worsen following SARS-CoV-2 infection. Although it is still unclear whether PD increases the susceptibility to SARS-CoV-2 infection or whether COVID-19 increases the risk of or unmasks future cases of PD, emerging evidence sheds more light on the molecular mechanisms underlying the relationship between these two diseases. Among them, angiotensin-converting enzyme 2 (ACE2), a significant component of the renin-angiotensin system (RAS), seems to play a pivotal role. ACE2 is required for the entry of SARS-CoV-2 to the human host cells, and ACE2 dysregulation is implicated in the severity of COVID-19-related acute respiratory distress syndrome (ARDS). ACE2 imbalance is implicated in core shared pathophysiological mechanisms between PD and COVID-19, including aberrant inflammatory responses, oxidative stress, mitochondrial dysfunction, and immune dysregulation. ACE2 may also be implicated in alpha-synuclein-induced dopaminergic degeneration, gut–brain axis dysregulation, blood–brain axis disruption, autonomic dysfunction, depression, anxiety, and hyposmia, which are key features of PD.

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Smoking enhances the expression of angiotensin‐converting enzyme 2 involved in the efficiency of severe acute respiratory syndrome coronavirus 2 infection

Cited by 5 publications

References 35 publications

Long-term effects of extreme smoke exposure on COVID-19: A cohort study

Long-term effects of extreme smoke exposure on COVID-19: A cohort study

Long‐term effects of extreme smoke exposure on COVID‐19: A cohort study

Exploring the Role of ACE2 as a Connecting Link between COVID-19 and Parkinson’s Disease

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