← Lost Capybara Productions Evidence review · Aug 2026

Atmospheric & environmental triggers of atrial fibrillation

A graded evidence explorer: what has been linked in the published literature, how good those studies actually are, what has been tested after cardiothoracic surgery, and a candidate variable list for a cardiac-ICU study. Grades are GRADE-style confidence in the body of evidence for each exposure–outcome pair.

Pairs
catalogued across 11 domains
Graded HIGH
two of those are surrogate or device-physics endpoints
LOW / VERY LOW
the modal state of this literature
No evidence
never studied against the outcome

Confidence of the evidence, by domain

Each bar is the number of exposure–outcome pairs in that domain, segmented by confidence grade.

Search & filter
Confidence grade
Domain
Factor Arrhythmia / outcome Dir. Typical effect Studies Confidence Key studies & principal limitation

Solar storms, geomagnetic activity and electromagnetic fields

You asked for this specifically, so it gets its own treatment. The short version: one part of it is real and clinically actionable, and it is not the part people mean. Device electromagnetic interference is established physics. Ambient space weather as a cause of arrhythmia is not supported, and the largest dataset in existence points the opposite way.

What is established

  • CIED electromagnetic interference. MagSafe/magnet accessories trigger magnet mode in 72–100% of devices at ≤1 cm (Nadeem 2021, PMID 34074132; Censi 2022, PMID 35076120); smartwatch backs and charging pucks 23–30% (Wegner 2026, PMID 41404751); 433 adverse events during ablation in CIED patients, 68% electromagnetic (Sison 2026, PMID 41690440). Monopolar cautery remains the classic in-hospital source. Managed by the AHA statement (PMID 38984417) and EHRA consensus (PMID 36228183).
  • MRI. Magnetohydrodynamic T-wave distortion is universal; clinical arrhythmia under protocol is essentially absent (MagnaSafe, NEJM 2017; Meier 2024, PMID 38918179 — 929 scans with abandoned/epicardial leads, no major adverse cardiac event). Fringe-field magnet-mode activation is real (52% of pacemakers in vitro at 3 T).
  • Occupational ELF magnetic fields are null. Four large cohorts: arrhythmia death HR 0.94 (0.71–1.24) in 20,141 Swiss railway workers (PMID 18593477); pacemaker implantation RR 0.96 (0.81–1.14) in 24,056 Danish utility workers (PMID 12397004); total CVD HR 1.02 (0.99–1.06) in 120,852 (PMID 23322917).

The decisive arrhythmia dataset

Ebrille 2015, Mayo Clin Proc, PMID 25659238. ALTITUDE remote-monitoring database, 69,556 patients, 86,427 ICD shocks and 631,193 shock+ATP events, 2009–2012, geomagnetic activity in four levels.

Shocks per 1,000 patients per day fell monotonically from 1.29 ± 0.47 on quiet days to 0.94 ± 0.29 on storm days (P<.001); shocks+ATP 9.29 → 7.83 (P=.008).

The association is inverse. The single best-powered ventricular-arrhythmia dataset ever assembled shows fewer arrhythmia therapies during geomagnetic storms. Any hypothesis that storms trigger arrhythmia has to explain this first.

For atrial fibrillation specifically there is no adequately powered main-effect study at all. The most-cited paper (Zilli Vieira 2022, Europace, PMID 34791174) has 51 patients contributing 335 AF episodes, and space weather enters only as an effect modifier of air-pollutant associations across roughly 45 interaction tests with overlapping confidence intervals.

The physics problem, quantified

  • Earth's static field at the surface is 25–65 µT. A severe geomagnetic storm (Dst ≈ −589 nT, March 1989) perturbs it by about 1%; a typical "storm day" by 0.2–0.5%. Walking past steel reinforcement changes your local field by more.
  • Induced tissue electric field, Faraday, torso loop r = 0.1 m, aggressive substorm dB/dt = 500 nT/min: E ≈ 4 × 10−10 V/m. The ICNIRP basic restriction for CNS tissue is 0.1 V/m — roughly 109 times larger. Myocardial capture needs ~1–10 V/m. Membrane thermal noise is many orders above the induced signal.
  • Magnetohydrodynamic potentials scale linearly with B. The 1–10 mV MHD artefact seen at 7 T scales to about 0.7 nanovolts at 500 nT. That is not a mechanism.
  • Radical-pair/cryptochrome transduction requires either far higher intensity or radical-pair lifetimes >1 µs, "far longer than lifetimes typically observed in condensed matter" (Krylov 2026, Biol Rev, DOI 10.1111/brv.70108). ELF fields with periods >3.33 ms are quasi-static over a radical pair's lifetime, so a slow storm signal offers nothing to rectify.

Why the positive literature looks the way it does

  1. The exposure is planetary. Kp/Ap/Dst is identical for everyone on Earth that day. There is no exchangeable unexposed group; even nominally individual-level case-crossover designs (Feigin 2014, PMID 24757102) carry a purely ecological exposure inside them.
  2. Adverse seasonal confounding. Geomagnetic activity peaks at the equinoxes (Russell–McPherron) and cycles at 27 days and 11 years. Cardiovascular events peak in winter and follow temperature, infection, pollution and daylight. The exposure signal lives in the same frequency band as the confounders being smoothed out.
  3. Multiplicity of 103–104. ~6–10 indices × ~5–10 lags × 4–8 outcomes × 4–8 strata, with no correction anywhere in the field.
  4. Uncorrected autocorrelation. Mattoni 2020 (Eur J Appl Physiol, PMID 32306151) repeated the HRV analysis properly: "the loss of most significant effects after this correction suggests that previous findings may be a result of autocorrelation… we question the validity of the previous studies."
  5. Sign incoherence. The same index is claimed to increase stroke, decrease ICD shocks, increase MI, decrease HRV and increase parasympathetic tone, depending on the group analysing it.
  6. Author concentration. Four clusters (Stoupel; Halberg–Cornélissen; Vencloviene/Kaunas; HeartMath/Global Coherence) produce most positive reports, sharing data infrastructure and analytic conventions. Counting their papers as independent replication is a category error.
  7. Publication bias. A 2025 scoping review found 28 of 36 studies (78%) positive — an implausible hit rate for a field with no mechanism and mostly ecological designs. The 2025 meta-analysis (PMID 40256184) included only 6 of 644 screened studies and reports ranges rather than a pooled estimate with I².
  8. Effect sizes incompatible with the exposure. A claimed ~3-fold MI increase in women from a 0.2% field perturbation should reduce credence, not raise it.

If you wanted to test it properly anyway

  1. Pre-register one primary triple — one exposure, one lag, one outcome. Everything else FDR-controlled against a published grid.
  2. Use local measured fields, not planetary indices: nearest INTERMAGNET observatory dB/dt and local K.
  3. Exploit the magnetic-latitude gradient. A real effect must be larger at high magnetic latitude, where perturbations are 5–10× greater. The northern-Sweden null (PMID 12135204) is a direct failure of that prediction and any positive claim must account for it.
  4. Time-stratified case-crossover with same-month, same-weekday referents, plus explicit adjustment for temperature, PM2.5 and influenza activity.
  5. Negative controls, pre-specified. Exposure: Kp shifted six months, or future exposure. Outcome: hip-fracture admissions or another endpoint sharing the care-seeking pathway with no plausible geomagnetic route.
  6. Autocorrelation-aware inference — pre-whitening, AR error structure, or block-bootstrap. Naive correlation of two time series is inadmissible.
  7. Power for a defensible effect. At OR ≤ 1.05 with ~2% exposed days, you need on the order of 105–106 events. Every study except Ebrille is underpowered by 2–3 orders of magnitude for any effect that is not biophysically incredible.
  8. A sham-controlled human exposure experiment at realistic amplitudes (≤500 nT with a realistic dB/dt spectrum on a normal 50 µT background) does not currently exist. Every "simulated storm" study uses supraphysiological amplitudes, unstated N, or no sham arm.
Practical bottom line for a cardiac ICU: act on device EMI (phones and magnetic accessories >15 cm from the generator, bipolar cautery, ipsilateral return pads, MRI protocols). Do not staff, schedule, or prophylax against Kp forecasts.

Post-cardiothoracic surgery and the cardiac ICU

POAF occurs in ~30% overall (20% isolated CABG, 40–50% valve or combined), peaks on POD 2–4, and ~90% of episodes fall within six postoperative days. The mechanistic model is substrate plus trigger — atrial remodelling and pericardial inflammation, acted on by autonomic surge, oxidative stress and electrolyte shift. That model is explicitly permissive of circadian and environmental modulation, which makes the emptiness of the table below notable rather than reassuring.

What has actually been studied

  • Time of day of surgery. Montaigne 2018 (Lancet, PMID 29107324) found lower perioperative myocardial injury with afternoon surgery (RCT geometric mean ratio 0.79, 0.68–0.93) via Rev-Erbα. AF was not an endpoint. Four independent failures to replicate plus a null pooled meta-analysis (PMID 41412842). The single AF datum anywhere in this literature is 20.6% AM vs 21.4% PM — null.
  • Season of surgery. One study reports POAF by season (n=681, single centre, single pandemic year): 0% / 1.6% / 1.6% / 2.1%, p=0.139. A POAF rate of 0–2.1% against an expected 20–40% is catastrophic ascertainment failure. Effectively unstudied.
  • Lunar phase. Two papers, neither with AF as an outcome. Shuhaiber 2013 (n=210) reports full-moon mortality OR 0.21 (0.05–0.81) across ≥16 uncorrected comparisons — read it as a false positive. Bjursten 2022 (n=2,995, PMID 34450636) is a well-built day-of-week-matched case-crossover whose primary comparison is null (RR 1.08, p=0.057) and whose cleanest exposure definition is also null. Its value to you is as a design template, not as evidence.
  • Chronic altitude. POAF after cardiac surgery above vs below 1,500 m: OR 1.07 (0.71–1.60), null (PMID 34143663).
  • Air pollution after CABG. Two cohorts use long-term mortality or MACE; neither has AF as an outcome. The one CABG mortality study reports NO₂ HR 2.70 (2.03–3.59), which is implausibly large for an air-pollution mortality effect and points at uncontrolled urbanicity/deprivation confounding.
  • Geomagnetic activity in open-heart surgery. One prospective cohort (n=233 CABG/valve) exists — and it measured psychological symptom scores, not arrhythmia, despite the rhythm data presumably being available.
  • ICU environment. Noise, light, circadian disruption and melatonin have been studied against sleep and delirium. Arrhythmia appears as an endpoint nowhere. The ATS research statement on ICU sleep and circadian disruption lists it as a blank space in its own agenda.

Genuine gaps — never studied against POAF

  1. Circadian timing of the POAF event itself. The hour-of-day distribution of first AF onset in cardiac surgical patients has never been described — despite every patient being on continuous telemetry with timestamped alarms. No external data, no linkage, no de-identification obstacle. lowest hanging fruit
  2. PM2.5 / NO₂ / O₃ during the POD 0–5 at-risk window. Maps exactly onto the Link 2013 device case-crossover design (PMID 23770178), in a cohort under continuous monitoring. highest yield
  3. Pre-operative pollution exposure window (7/30/365 d) vs POAF.
  4. Ambient temperature, barometric pressure, humidity, frontal passage on the day of surgery or on postoperative days. Drier air is a documented paroxysmal-AF trigger in the community (PMID 25756220) and has never been tested here.
  5. Measured ICU noise (dB) vs POAF. ICU LAeq runs 47–51 dB with LAmax to 99 dB — well inside the band where the transportation-noise and experimental-noise literature show acute cardiovascular effects, via exactly the arousal → catecholamine → sleep-fragmentation mechanism implicated in POAF. The two literatures have never been joined.
  6. Measured ICU light / lux / melanopic EDI, melatonin rhythm, objectively measured sleep fragmentation vs POAF. Only exogenous melatonin as a drug has been trialled.
  7. Rewarming rate and core-temperature trajectory after hypothermic CPB vs POAF — clinically actionable and essentially unindexed.
  8. Single-occupancy vs open-bay room design; ambient room temperature; hospital elevation; day of week; DST transitions; photoperiod.
  9. Delirium and POAF as manifestations of a shared environmental cause. Their co-occurrence is documented in DECADE sub-analyses but is always modelled as patient-level confounding, never as shared exposure.
  10. Geomagnetic/solar activity vs POAF — unstudied, and worth including only as a pre-registered low-prior arm with negative controls.

The data-linkage obstacle, verified

If you were hoping to do this in a public ICU dataset: date-shifting destroys weather and air-quality linkage in every one of them.

  • MIMIC-III / MIMIC-II — dates shifted per patient, but documentation explicitly states "the day of the week and season of the year were preserved." So season, day-of-week and hour-of-day analyses are legitimate; daily weather is not.
  • MIMIC-IV — a single shift per subject_id, into 2100–2200; distinct patients are "not temporally comparable." Seasonality preservation is not asserted in the documentation (an open question in the MIT-LCP issue tracker). Treat season as unrecoverable until confirmed. anchor_year_group gives only a 3-year window.
  • HiRID — the standout: documentation explicitly guarantees "we made sure to preserve the seasonality, time of day and the day of the week." Best free external validation cohort for season/hour/day-of-week hypotheses.
  • eICU-CRD — hospital and unit identifiers removed; region only. AmsterdamUMCdb — millisecond offsets from admission, no dates.

Consequence: a daily weather or air-quality analysis is executable only on your own institutional registry with intact admission dates and a hospital geocode, or on a national registry (STS ACSD, EACTS, ANZSCTS, SWEDEHEART, NICOR) under a data agreement that retains dates. The proof of concept for ICU-to-monitor linkage already exists: Groves 2020 (PMID 32355989) linked 46,965 emergency ICU episodes across 87 ANZ ICUs to EPA monitors — PM2.5 per 10 µg/m³ → 30-day mortality RR 1.18 — but had no arrhythmia endpoint.

The POAF-specific bias you must design around. Continuous ECG monitoring detects substantially more POAF than daily 12-lead review. Telemetry duration co-varies with ICU length of stay, which co-varies with case complexity, weekday of surgery and staffing. Any exposure correlated with length of stay — weekend surgery, winter surgery, an afternoon list running late — will generate a spurious POAF association purely through longer monitoring. Model person-hours-at-risk explicitly, log telemetry gap minutes, and treat ascertainment intensity as a time-varying covariate rather than a limitation paragraph.

Candidate studiable variables

Broader than what has been published — this is the design space. Ordered by how much genuine contrast the variable actually has inside a climate-controlled, filtered-air, artificially-lit ICU box, because that ordering should decide your primary exposure, not which variable is most interesting.

Tier A — measured inside the unit, large within-ICU contrast, essentially unstudied

  • Sound. Bedside LAeq,1min, LAmax, number of night-time events >45 dB(A), alarm counts by type and source, conversation vs equipment fraction. Use event counts, not Lden-style averages — the randomised human data show the vascular effect scales with the number of events, not with equivalent level.
  • Light. Bedside illuminance and melanopic EDI at eye level, full 24-h profile, day/night ratio, lights-on event count, window proximity, blind position.
  • Circadian and sleep. Actigraphy or EEG-derived sleep fragmentation, night-time care-interaction density, urinary 6-sulfatoxymelatonin and cortisol rhythm, RASS trajectory, CAM-ICU delirium as a shared-cause co-outcome.
  • Thermal. Bedside room temperature and RH; patient core-temperature trajectory, rewarming rate after hypothermic CPB, time to normothermia, fever burden, hypothermia overshoot.
  • Indoor air. Indoor PM2.5 and PM1 (optical with gravimetric calibration), CO₂ as an air-exchange proxy, NO₂, VOCs; compute and report the infiltration factor Finf for your unit empirically.
  • Respiratory / oxygen. FiO₂ and SpO₂ trajectory, hyperoxia hours, desaturation burden (a T90 analogue), ventilation mode and PEEP as an intrathoracic-pressure and atrial-stretch term.
  • Built environment. Single room vs open bay, bed position relative to door and nursing station, distance to the busiest alarm source.
  • Excursions. Transport episodes to CT/cath lab/OR — flag or model separately; these are the only times the patient leaves the box.

Tier B — external environment (requires intact dates plus a hospital or residential geocode)

  • Air quality: PM2.5, PM10, PMcoarse, ultrafine particle number, black carbon, NO₂, NOx, O₃, SO₂, CO; PM speciation (sulfate, nitrate, ammonium, organic matter) where available; AQI category; wildfire-smoke days (satellite smoke-specific PM2.5, not total); dust-event flags. Windows: pre-operative 7/30/365 d and postoperative 0–5 d, modelled as a lag surface rather than a chosen lag.
  • Meteorology: mean/min/max temperature, apparent temperature, wet-bulb globe temperature, heat-wave and cold-spell indicators, diurnal temperature range, day-to-day change, absolute and relative humidity, barometric pressure and its 24-h change, wind speed, frontal passage, precipitation, sunshine hours, photoperiod at latitude.
  • Residential exposures (pre-admission): modelled Lden and Lnight at the home address, artificial light at night, greenspace/NDVI, area deprivation, distance to major road.
  • Biological aerosols: pollen counts by taxon, mould spore counts.
  • Infection activity — mandatory, not optional: sentinel ILI rate, influenza/RSV/COVID laboratory positivity or wastewater surveillance. This is the dominant time-varying confounder for every winter-peaking exposure and almost no AF study adjusts for it.
  • Site-level: hospital elevation, urban heat island index, climate zone (multicentre only).

Tier C — temporal and cyclical (free to compute, no linkage required)

  • Hour of day of surgery start and of cross-clamp release; hour of day of AF onset; postoperative hour and day.
  • Day of week; weekend vs weekday; public holiday; proximity to a DST transition; academic-calendar turnover.
  • Month, season, calendar year (secular trend), and time since the start of the surgical programme.
  • Lunar phase and illumination fraction — include it, but pre-specify it as a negative control rather than a hypothesis. If it comes up "significant" in your model, that is information about your multiplicity, not about the moon.

Tier D — space weather (include only pre-registered, with negative controls)

  • Local ground-magnetometer dB/dt and local K from the nearest INTERMAGNET observatory — not planetary Kp.
  • Dst minimum, Ap, storm-day classification, AE index.
  • Solar wind speed, IMF Bz, F10.7, sunspot number; solar flare class and timing; solar proton events.
  • Neutron-monitor count rate and Forbush-decrease flags (anticorrelated with solar activity).
  • Pre-specified negative-control exposure (Kp shifted six months, or future-lagged exposure) and negative-control outcome (an endpoint sharing the detection pathway with no plausible geomagnetic route). A non-null negative control quantifies your residual confounding directly — which is the only genuinely useful thing this arm can produce.
  • Magnetic-latitude gradient across sites, if multicentre.

Tier E — the covariates without which none of the above is interpretable

Postoperative hour (the dominant driver — risk peaks at 48–72 h), beta-blocker and amiodarone administration timing and dose, beta-blocker withdrawal, magnesium and potassium, CRP/IL-6/white cell count, fluid balance, inotrope and vasopressor dose, haemoglobin, pain score, sedation depth, mechanical ventilation status, temporary epicardial pacing mode and rate (it both masks AF detection and is itself adjusted in response to rhythm), CPB and cross-clamp time, left atrial diameter, prior paroxysmal AF, and — critically — telemetry gap minutes and artefact fraction per hour as the ascertainment-intensity term.

Ranked by expected within-ICU contrast, the exposures that actually vary for an inpatient are: noise (survives the envelope entirely, and is mostly generated indoors) → light and circadian disruption (entirely indoor) → room temperature → CO₂/air exchange → indoor-generated particles → infiltrated outdoor PM (heavily attenuated) → outdoor gases (mostly scrubbed). That ordering, not topical interest, should pick your pre-specified primary exposure.

How the grades were assigned

GRADE-style, adapted for environmental health (Morgan 2016, PMID 26827182): observational exposure studies start high because randomisation is impossible, then are downgraded for risk of bias. Given how severe exposure assignment is in this field, MODERATE is the realistic ceiling for any single study.

Downgrade one level for each (floor VERY LOW)

  1. Exposure assignment. Nearest-monitor or single-city monitor with no infiltration/time-activity adjustment: −1. Ecological exposure with no within-population contrast (geomagnetic indices, city-wide series): −2.
  2. Outcome ascertainment. ICD-code hospitalisation or ED discharge diagnosis only: −1. Self-report or death certificate: −2. No downgrade for adjudicated device electrograms or continuous telemetry.
  3. Confounding. No adjustment for temperature and co-pollutants and (where relevant) noise: −1. No control for season or long-term trend: −2.
  4. Multiplicity. No pre-registration and a selected lag reported without the full lag–response curve: −1. Positive finding confined to a subgroup with a null main effect: a further −1.
  5. Imprecision. CI includes 1.00, or the E-value for the CI limit nearest the null is <1.25: −1.
  6. Small-study effects. Fewer than 10 comparable studies in the literature and an effect larger than the largest study: −1.

Upgrade one level for each (cap HIGH)

  • Monotone dose–response across ≥3 categories or a DLNM curve robust to df sensitivity.
  • Within-person self-matched design with device- or telemetry-level outcome ascertainment.
  • Quasi-experimental exposure contrast (HEPA RCT, factory closure, traffic restriction, defined smoke episode).
  • Pre-registered primary exposure–lag–outcome triple with FDR control.

The E-value problem — the single most important number here

The E-value is the minimum association an unmeasured confounder would need with both exposure and outcome to explain the finding away: E = RR + √(RR × (RR−1)).

Pooled estimateE-value (point)E-value (CI limit)
RR 1.011 — railway noise & AF /10 dB1.111.05
RR 1.018 — PM2.5 & AF, short-term1.15~1.00
RR 1.02 — PM2.5 & ventricular arrhythmia1.161.11
RR 1.027 — aircraft noise & AF /10 dB1.191.09
RR 1.05 — noise & AF, umbrella1.281.16
RR 1.11 — PM2.5 & AF, older adults1.461.21

An unmeasured confounder associated with both exposure and AF by a risk ratio of only 1.16–1.28 nullifies most of this literature. Candidates that easily exceed that and are routinely unmeasured: short-term alcohol intake, acute respiratory infection, sleep deprivation, physical exertion, ambient noise, indoor smoking, OSA severity, psychological stress — every one of them plausibly correlated with high-pollution days.

The E-values in this literature are smaller than the confounding that is known to exist.

Design hierarchy for trigger questions

  • Device / telemetry interrogation studies are the reference design. Machine-adjudicated outcome with second-level timestamps, no care-seeking filter, genuine hour-level lag resolution, natural within-person design, exact person-time. Their own threats: highly selected populations on antiarrhythmics, device classifications that are not diagnoses (undersensing at high rates, far-field oversensing, manufacturer-specific mode-switch thresholds), and small N inflating winner's curse.
  • Time-stratified case-crossover removes all time-invariant confounding by construction but is silent on anything varying over days to weeks — temperature, co-pollutants, pollen, influenza, weekend alcohol.
  • Time-series with DLNM is the right tool for lag surfaces, but the degrees-of-freedom-for-time choice directly determines the estimate, and knot placement × max lag × centring multiplies the researcher's choice space. Demand a sensitivity sweep across 3–12 df/year.
  • Ecological/correlational designs — the geomagnetic literature's mainstay — are disqualifying here, not merely weak.

Power, honestly

Self-matched design, exposure standardised within stratum, 3 control periods per case, α=0.05, 80% power. Required events, not patients:

Target OR per 1 SDEvents requiredSingle 1,000-case/yr programme
1.20≈ 315≈ 1 year
1.15≈ 550≈ 1.5–2 years
1.10≈ 1,200≈ 3–4 years
1.05≈ 4,400≈ 12–15 years — needs a consortium

Three corrections make that worse. (1) Infiltration. Indoor PM2.5 in air-conditioned space runs Finf ≈ 0.47 ± 0.18, and 0.09–0.27 in HVAC commercial buildings; a true OR of 1.20 per SD of indoor exposure becomes ≈1.06 per SD of outdoor exposure, moving you from 315 events to ~3,000. Measuring indoor exposure is worth more than a tenfold increase in sample size. (2) Within-stratum variance is small in a climate-controlled room — pilot it for three months and use the observed σ, not 1. (3) Adjudication attrition and telemetry gaps cost 10–25% of usable events.

The honest framing for a protocol: a single-centre ICU study is powered only for OR ≥ 1.15–1.20 per SD — larger than any effect reported in the ambient literature. Design and pre-register it as a noise / light / temperature study, where within-ICU contrast is genuinely large, and/or as an exposure-characterisation and feasibility study that generates the Finf and σwithin parameters a consortium would need. Not as a definitive PM2.5–POAF study.

Caveats you need before citing any of this

Search limitations

  • The NCBI E-utilities API and PubMed/PMC pages were not reachable from this environment (403 on eutils; reCAPTCHA on PubMed/PMC; Europe PMC, Crossref, OpenAlex and Semantic Scholar likewise blocked or heavily rate-limited). Retrieval used web search, direct publisher sites (OUP, Springer/BMC, Nature, MDPI, Frontiers, LWW, J-Stage), DOAJ, institutional repositories, and a Wiley-weighted academic corpus.
  • Consequence: this is a comprehensive structured review, not a PRISMA-reproducible systematic search. Study counts per exposure are indicative rather than de-duplicated screening outputs.
  • PMIDs. No PMID here is invented. Where a PMID appeared verbatim in a resolved PubMed URL or fetched text it is given plainly; a number of citations were verifiable only by DOI. Verify every PMID and every effect estimate against the primary record before it goes into a manuscript, grant or protocol. Elsevier, AHA and JACC full texts were largely inaccessible, so several effect estimates came from abstracts or secondary sources.
  • The web-search budget for this session was exhausted before an independent verification pass could be run.

Where the two independent appraisals disagreed

  • Short-term PM2.5 → AF. The substantive review graded it MODERATE (consistent direction, meta-analytic support, plausible HRV mechanism). The methodological review graded it LOW (pooled AF estimate rests on 4 studies, the best-measured device subgroup is null for ventricular arrhythmia, E-value 1.15–1.46, no synthesis has ever applied GRADE, and the umbrella review states arrhythmia is the thinnest stratum in environmental cardiology). Rows where this applies are flagged CONTESTED.
  • Cold → AF. Graded MODERATE on the strength of two very large Chinese case-crossover/DLNM studies; a methodological reading puts it at VERY LOW because there is no AF-specific meta-analysis, the parent syntheses run I² ≈ 93–99%, and the best-adjusted temperate-climate study is null.
  • Noise → AF. MODERATE from the pooled Nordic cohort; LOW from the umbrella-review perspective (WHO never graded AF; 64% of the underlying meta-analyses were rated LOW or VERY LOW by the umbrella's own GRADE).

Where they disagreed, the table shows the higher grade with the contested flag, so you can see both readings rather than a laundered consensus.

Specific numbers not to use

  • Zhang 2026, Heart (UK Biobank): HR 1.37 per 1 µg/m³ PM2.5 for AF, implying HR ≈ 25 per 10 µg/m³, with a CI width of 0.02 on 28,977 events. Not biologically credible; almost certainly a units or specification error. The downstream claim that 26–52% of AF cases are PM2.5-preventable should be treated as artefactual. Two other analyses of the same cohort report HR 1.044 per IQR and HR 1.26 per 10 µg/m³.
  • Shuhaiber 2013 full-moon mortality OR 0.21 (0.05–0.81) — n=210, ≥16 uncorrected comparisons, no mechanism, no replication.
  • Ho 2022's "8% OHCA reduction per 1 µg/m³" — internally inconsistent with the paper's own RR of 1.022 per 10 µg/m³.
  • Any geomagnetic effect size implying a large biological response to a 0.2–1% field perturbation.

Priority full texts to pull before writing anything

  1. PMID 35138681 — de Bont umbrella review; the load-bearing citation that AF/arrhythmia is the thinnest stratum in environmental cardiology.
  2. DOI 10.1161/JAHA.123.030907 — POAF ascertainment meta-analysis (assessment method and definition). Essential for your methods section.
  3. DOI 10.1161/CIRCRESAHA.123.323477 — "Environmental Exposome and Atrial Fibrillation," Circ Res 2024. Best single framing citation.
  4. DOI 10.1016/j.jcrc.2021.09.006 — circadian variation in new-onset AF in ICU patients; as far as I can tell the only paper directly on circadian timing of ICU NOAF onset.
  5. PMID 25659238 (Ebrille) and PMID 32306151 (Mattoni) — the two results that should anchor any space-weather section.
  6. PMID 29470452 (WHO/van Kempen) — the only body that applied GRADE outcome-by-outcome to environmental noise.
  7. PMID 28693043 — E-value methodology.
  8. NCT03503812 (MEDEA) — randomised dust-avoidance intervention with device-measured AF burden as a primary outcome. Results were not locatable; check the registry directly. This is the closest existing trial to the design you would want.