N-acetyl-cysteine (NAC) & Respiratory Health

Table of Contents

1. Mucolytic and Antioxidant Mechanism
2. COPD: BRONCUS, PANTHEON, HIACE, and the Cochrane Review
3. Chronic Bronchitis
4. Cystic Fibrosis
5. Idiopathic Pulmonary Fibrosis
6. Bronchiectasis
7. Influenza and Viral Respiratory Infection
8. Asthma
9. Pneumonia and ICU / Ventilator Settings
10. Doses Used in Studies and on the Label
11. Safety
12. Key Research Papers
13. Connections
14. Featured Videos

Mucolytic and Antioxidant Mechanism

Chemical Scissors on Mucus

Mucus in the airway is dominated by large glycoprotein polymers called mucins (principally MUC5AC and MUC5B) cross-linked by disulfide bonds between cysteine residues. NAC's free thiol can break these S–S bonds by thiol-disulfide exchange. Sheffner's 1963 laboratory paper (Ann NY Acad Sci) reported that NAC reduced the viscosity of mucoprotein solutions in vitro; this mucolytic action is the basis of its original respiratory use.

Glutathione in Airway Lining Fluid

The fluid lining the lower airways contains large amounts of glutathione: in healthy people, total glutathione in this epithelial lining fluid was 140-fold higher than in their plasma, and cigarette smokers had 80% higher levels than nonsmokers (Cantin 1987). In young adults with cystic fibrosis, reduced glutathione was low both in lining fluid and in plasma (Roum 1993). In a small bronchoscopy study, Bridgeman 1991 (Thorax) gave NAC 600 mg a day by mouth for five days; intact NAC was not detected in plasma or lavage fluid, but reduced glutathione was higher in plasma and lavage fluid than in untreated controls when lavage was done 1–3 hours after the last dose. The authors read this as rapid conversion of NAC to cysteine, with a temporary rise in the lung's antioxidant capacity.

Direct Free-Radical Scavenging

Reviews describe NAC as acting both as a glutathione precursor and as a direct scavenger of reactive oxygen species (Sadowska 2007; Dekhuijzen 2004); another review argues that its antioxidant benefit depends mainly on replenishing glutathione in cells that are deficient in it (Rushworth 2014). In a cell-culture study, oxidative stress and activated neutrophils switched on MUC5AC mucin production through the EGF receptor, and NAC blocked the neutrophil-driven effect (Takeyama 2000) — a laboratory finding that links oxidative stress to mucus production as well as to mucus thickness.

COPD: BRONCUS, PANTHEON, HIACE, and the Cochrane Review

COPD trials of NAC have measured two main things: the rate of lung-function decline and the number of exacerbations (flare-ups). BRONCUS found no effect on lung-function decline. Results on exacerbations differ between trials, doses and reviews, as set out below.

BRONCUS Trial (Decramer 2005)

523 patients with COPD at 50 centres were randomized to NAC 600 mg once daily or placebo and followed for 3 years. The yearly decline in FEV1 did not differ (54 versus 47 mL), and neither did the number of exacerbations per year (1.25 versus 1.29; hazard ratio 0.99). A subgroup analysis suggested fewer exacerbations with NAC in patients not using inhaled corticosteroids. The authors concluded that NAC at this dose was ineffective at preventing lung-function deterioration and exacerbations (Lancet 365:1552).

PANTHEON Trial (Zheng 2014)

At 34 hospitals in China, 1,006 patients aged 40–80 with moderate-to-severe COPD were randomized to NAC 600 mg twice daily or placebo for 1 year. The exacerbation rate was 1.16 per patient-year with NAC versus 1.49 with placebo (risk ratio 0.78, 95% CI 0.67–0.90, p=0.0011). Adverse events were reported in 29% of the NAC group and 26% of the placebo group. The authors concluded that the benefit was seen especially in moderate disease and that mild COPD needed further study (Lancet Respir Med 2(3):187). This is a trial result in one population, not an established dose.

HIACE Trial (Tse 2013)

A single-hospital trial in Hong Kong randomized 120 patients aged 50–80 with stable COPD to NAC 600 mg twice daily or placebo for 1 year. NAC improved small-airway measures (FEF25–75 and forced oscillation) and reduced exacerbation frequency (0.96 versus 1.71 per year, P=.019); the reduction in hospital admissions (0.5 versus 0.8 per year) was not significant, and breathlessness score, quality-of-life score and 6-minute walk distance did not differ (Chest 144:106).

Cochrane Review (Poole 2019)

This review covers all oral mucolytics, not NAC alone (NAC, carbocysteine, erdosteine, ambroxol and others): 38 trials with 10,377 participants. In 28 studies (6,723 participants), people given a mucolytic were more likely to stay exacerbation-free (Peto odds ratio 1.73, 95% CI 1.56–1.91; moderate-certainty evidence), with a number needed to treat of 8 over an average of nine months. Heterogeneity was high, more recent and longer studies showed smaller effects than earlier and shorter ones, and the type or dose of mucolytic did not seem to change the effect size. The review found limited impact on lung function and quality of life, and results too imprecise to say whether mortality is affected. The authors describe the benefit as a small reduction in the likelihood of an exacerbation.

The Dose Question

Reviews disagree on whether dose matters. The Cochrane review above found no clear effect of dose. A 2015 meta-analysis of 13 NAC studies (4,155 patients) found fewer exacerbations with NAC overall (relative risk 0.75, 95% CI 0.66–0.84), an effect more apparent in patients without airway obstruction; in patients with spirometry-confirmed COPD, doses above 600 mg a day were also effective (relative risk 0.75). Its authors concluded that people with documented airway obstruction need at least 1,200 mg a day for this effect (Cazzola 2015).

Chronic Bronchitis

Chronic bronchitis is defined as a productive cough on most days for at least 3 months a year in 2 consecutive years.

Stey Systematic Review 2000

Of 39 trials retrieved, 11 (2,011 patients, published 1976–1994) met the review's criteria (Eur Respir J 16:253). Over treatment periods of about 12–24 weeks, 48.5% of patients taking NAC had no exacerbation versus 31.2% on placebo (relative benefit 1.56; number needed to treat 5.8). In five trials, 61.4% of NAC patients reported improved symptoms versus 34.6% on placebo (number needed to treat 3.7). Gastrointestinal side effects were reported by 10.2% on NAC and 10.9% on placebo. The authors left open whether the benefit justifies routine long-term use.

Grandjean Meta-Analysis 2000

Nine double-blind, placebo-controlled trials qualified (Clin Ther 22:209). Most used 600 mg a day (one used 400 mg, one 1,200 mg), mostly for about 6 months. In the trials that counted exacerbations, NAC was associated with a 23% decrease in the number of acute exacerbations compared with placebo.

In much of Europe NAC has long been sold over the counter as a mucolytic.

Cystic Fibrosis

CF airways show marked neutrophil-dominated inflammation, and people with CF have low reduced glutathione both in airway lining fluid and in plasma (Roum 1993). NAC has been studied for both mucus thinning and antioxidant effects.

The Cochrane Review of Thiol Drugs in CF

A 2013 Cochrane review identified nine trials (255 participants) of nebulized or oral thiol derivatives, including NAC; seven were more than 10 years old. The treatments were generally well tolerated, but the review found no evidence of significant clinical benefit in its primary outcomes for either route, and very few good-quality trials (Tam 2013). The review's background names dornase alfa and nebulized hypertonic saline as the muco-active therapies used in CF.

Oral High-Dose NAC

• Tirouvanziam 2006 (PNAS): in a phase 1 study in 18 CF patients, NAC 0.6–1.0 g three times daily for 4 weeks improved blood-neutrophil glutathione and lowered sputum elastase activity and airway neutrophil counts. Lung function did not improve over this short course.
• Conrad 2015 (J Cyst Fibros): in a randomized, placebo-controlled phase II trial, 70 CF patients took NAC or placebo three times daily for 24 weeks. Lung function (FEV1 and FEF25–75) stayed stable or rose slightly with NAC and fell with placebo (FEV1 treatment effect 150 mL, p<0.02), but sputum elastase — the primary outcome — and other inflammation markers did not differ.

Idiopathic Pulmonary Fibrosis

IPF is characterized by progressive fibrosis of the lung tissue. Oxidative stress has been proposed as part of its mechanism, and a combination of prednisone, azathioprine and NAC was widely used before it was tested against placebo (Raghu 2012).

IFIGENIA 2005

Demedts randomized 182 IPF patients, all taking prednisone plus azathioprine, to add NAC 600 mg three times daily or placebo for 1 year. At 12 months NAC had slowed the decline in vital capacity (difference 0.18 L, 9%) and DLco (24%); mortality did not differ significantly (9% versus 11%) (NEJM 353:2229).

PANTHER-IPF (2012 and 2014)

The IPF Clinical Research Network's PANTHER trial was reported in two stages:

• Combination arm (Raghu 2012, NEJM): the three-arm trial compared prednisone + azathioprine + NAC, NAC alone, and placebo. At a planned interim analysis, the combination group had more deaths (8 versus 1, P=0.01) and hospitalizations (23 versus 7) than placebo, with no sign of benefit, and that arm was stopped at a mean follow-up of 32 weeks. The authors wrote that the findings provide evidence against the combination.
• NAC alone (Martinez 2014, NEJM): 264 patients (133 NAC, 131 placebo). At 60 weeks the change in FVC did not differ (−0.18 versus −0.19 L, P=0.77), nor did death (4.9% versus 2.5%) or acute exacerbation (2.3% in each group). NAC alone was null.

A post-hoc genetic analysis of PANTHER (Oldham 2015, AJRCCM) found that NAC was associated with fewer composite events in people with the TOLLIP rs3750920 TT genotype (hazard ratio 0.14) but a non-significant trend toward harm in those with the CC genotype (hazard ratio 3.23), replicated in a second cohort. The authors called for a genotype-stratified prospective trial before any recommendation on NAC in IPF.

Bronchiectasis

BENE Trial (Qi 2019)

At five hospitals in Shandong, China, 161 adults with bronchiectasis and at least two exacerbations in the past year were randomized to NAC 600 mg twice daily for 12 months or to on-demand treatment (there was no placebo). The exacerbation rate was 1.31 per patient-year with NAC versus 1.98 in the control group (risk ratio 0.41, 95% CI 0.17–0.66, P=0.0011); 24.7% versus 11.3% stayed exacerbation-free. Daily sputum volume fell and quality of life improved with NAC, and no severe adverse events were reported. The authors wrote that the results should be verified in a larger randomized trial (Respir Res 20:73).

Influenza and Viral Respiratory Infection

De Flora 1997

In a double-blind trial at 20 Italian centres, 262 people (78% aged 65 or over; 62% with chronic non-respiratory degenerative disease; people with chronic respiratory disease were excluded) were randomized to NAC 600 mg twice daily or placebo for 6 months over the winter (Eur Respir J 10:1535). NAC significantly reduced the frequency and severity of influenza-like episodes and the time spent in bed. NAC did not prevent infection — seroconversion to the A/H1N1 strain was similar in the two groups — but 25% of infected people taking NAC developed symptomatic illness, versus 79% on placebo. The authors also reported a shift in cell-mediated immunity from anergy toward normal responsiveness with NAC.

Laboratory and Animal Work

• Geiler 2010 (Biochem Pharmacol): in human lung cells infected with H5N1 influenza, NAC at 5–15 mM reduced cell damage, cell death and virus yield, and lowered production of CXCL8, CXCL10, CCL5 and IL-6, through inhibition of NF-kB and p38 signalling. This is a cell-culture study.
• Ungheri 2000 (Int J Immunopathol Pharmacol): in mice infected with influenza, oral NAC (1 g/kg a day) significantly decreased mortality. This is an animal study.

Asthma

Oxidative stress and mucus hypersecretion are proposed reasons to study NAC in asthma, but the clinical evidence is small.

• Millman 1985 (Ann Allergy): a short report that 10% acetylcysteine solution given together with a bronchodilator by pressure machine cleared airway secretions in asthmatic patients without inducing bronchospasm.
• Aliyali 2010 (Iran J Allergy Asthma Immunol): in a single-blind trial, 50 patients hospitalized with an asthma exacerbation received oral NAC 600 mg twice daily or placebo on top of standard treatment for 5 days. Wheeze, cough, breathlessness, sputum and sleep scores and morning peak flow did not differ; the authors concluded NAC had no significant effect.

Safety finding: inhaled NAC can cause bronchospasm. The US prescribing information for acetylcysteine inhalation solution states that clinically overt bronchospasm occurs infrequently and unpredictably, even in people with asthmatic bronchitis, that asthmatic patients using it are to be watched carefully, that most bronchospasm is quickly relieved by a nebulized bronchodilator, and that the drug is to be stopped if bronchospasm progresses (acetylcysteine solution label, DailyMed).

Pneumonia and ICU / Ventilator Settings

• Zhang 2018 (Medicine): in a randomized trial in community-acquired pneumonia, adding NAC 1,200 mg a day to conventional treatment lowered blood markers of oxidative stress (MDA) and inflammation (TNF-α) and raised total antioxidant capacity, but did not improve CT scores more than conventional treatment alone.
• Sharafkhah 2018 (Med Gas Res): in a double-blind trial in 60 mechanically ventilated ICU patients at high risk, NAC 600 mg twice daily by nasogastric tube was followed by less ventilator-associated pneumonia than placebo (26.6% versus 46.6%) and shorter ICU and hospital stays.
• Suter 1994 (Chest): in 61 patients with mild-to-moderate acute lung injury, intravenous NAC (40 mg/kg a day for 3 days) improved oxygenation and reduced the need for ventilator support at day 3 (17% versus 48% still ventilated), but did not significantly reduce progression to ARDS or 1-month mortality (22% versus 35%).
• Bernard 1997 (Chest): in 46 ventilated patients with ARDS, intravenous NAC or another glutathione precursor restored red-cell glutathione and shortened the duration of acute lung injury, with no difference in mortality (NAC 36%, placebo 40%); the authors called for larger studies.

Doses Used in Studies and on the Label

Oral

• Chronic bronchitis meta-analyses: trials mostly used 600 mg a day, for about 3–6 months (Grandjean 2000; Stey 2000)
• COPD trials: 600 mg once daily for 3 years in BRONCUS (no effect); 600 mg twice daily for 1 year in PANTHEON and HIACE
• Bronchiectasis: 600 mg twice daily for 12 months (BENE)
• IPF: 600 mg three times daily, added to prednisone and azathioprine (IFIGENIA)
• Cystic fibrosis: 0.6–1.0 g three times daily for 4 weeks (Tirouvanziam 2006)

Nebulized

• The US label for the 10% and 20% inhalation solution gives a usual dose of 3–5 mL of the 20% solution or 6–10 mL of the 10% solution, 3–4 times a day, by face mask, mouthpiece or tracheostomy

Bioavailability

In six healthy volunteers, the oral bioavailability of NAC was 4.0% for reduced NAC and 9.1% for total NAC (Olsson 1988). Much of an oral dose is converted to cysteine, the building block for glutathione; intact NAC was not detected in plasma or lung lavage fluid after oral dosing in Bridgeman's study.

Safety

• Odour: the label notes a slight disagreeable odour on administration
• Gastrointestinal effects: in the Stey review, gastrointestinal side effects were reported by 10.2% on oral NAC and 10.9% on placebo; in PANTHEON, adverse events of any kind occurred in 29% on NAC and 26% on placebo
• Bronchospasm with nebulized use — reported infrequently and unpredictably on the label, including in people with asthmatic bronchitis (see Asthma above)
• Label-listed adverse effects of the inhalation solution: stomatitis, nausea, vomiting, fever, runny nose, drowsiness, clamminess, chest tightness and bronchoconstriction
• Nitroglycerin interaction: in an unstable-angina trial, symptomatic hypotension occurred in 7 of 24 patients given NAC with intravenous nitroglycerin versus none of 22 given nitroglycerin alone (Horowitz 1988)
• Pregnancy: FDA Pregnancy Category B under the former letter system; the label reports that oral NAC was not teratogenic in a rabbit study at 500 mg/kg a day

Decisions about medicines and supplements belong with a clinician.

Key Research Papers

1. Sheffner AL. The reduction in vitro in viscosity of mucoprotein solutions by a new mucolytic agent, N-acetyl-L-cysteine. Ann N Y Acad Sci 1963;106:298–310. PubMed PMID: 13977050
2. Decramer M, Rutten-van Mölken M, Dekhuijzen PN, Troosters T, van Herwaarden C, Pellegrino R, et al. Effects of N-acetylcysteine on outcomes in chronic obstructive pulmonary disease (Bronchitis Randomized on NAC Cost-Utility Study, BRONCUS): a randomised placebo-controlled trial. Lancet 2005;365(9470):1552–60. PubMed PMID: 15866309
3. Zheng JP, Wen FQ, Bai CX, Wan HY, Kang J, Chen P, et al. Twice daily N-acetylcysteine 600 mg for exacerbations of chronic obstructive pulmonary disease (PANTHEON): a randomised, double-blind placebo-controlled trial. Lancet Respir Med 2014;2(3):187–94. PubMed PMID: 24621680
4. Tse HN, Raiteri L, Wong KY, Yee KS, Ng LY, Wai KY, et al. High-dose N-acetylcysteine in stable COPD: the 1-year, double-blind, randomized, placebo-controlled HIACE study. Chest 2013;144(1):106–118. PubMed PMID: 23348146
5. Poole P, Sathananthan K, Fortescue R. Mucolytic agents versus placebo for chronic bronchitis or chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2019;5(5):CD001287. PubMed PMID: 31107966
6. Stey C, Steurer J, Bachmann S, Medici TC, Tramèr MR. The effect of oral N-acetylcysteine in chronic bronchitis: a quantitative systematic review. Eur Respir J 2000;16(2):253–62. PubMed PMID: 10968500
7. Grandjean EM, Berthet P, Ruffmann R, Leuenberger P. Efficacy of oral long-term N-acetylcysteine in chronic bronchopulmonary disease: a meta-analysis of published double-blind, placebo-controlled clinical trials. Clin Ther 2000;22(2):209–21. PubMed PMID: 10743980
8. Tirouvanziam R, Conrad CK, Bottiglieri T, Herzenberg LA, Moss RB, Herzenberg LA. High-dose oral N-acetylcysteine, a glutathione prodrug, modulates inflammation in cystic fibrosis. Proc Natl Acad Sci U S A 2006;103(12):4628–33. PubMed PMID: 16537378
9. Conrad C, Lymp J, Thompson V, Dunn C, Davies Z, Chatfield B, et al. Long-term treatment with oral N-acetylcysteine: affects lung function but not sputum inflammation in cystic fibrosis subjects. A phase II randomized placebo-controlled trial. J Cyst Fibros 2015;14(2):219–27. PubMed PMID: 25228446
10. Demedts M, Behr J, Buhl R, Costabel U, Dekhuijzen R, Jansen HM, et al. High-dose acetylcysteine in idiopathic pulmonary fibrosis. N Engl J Med 2005;353(21):2229–42. PubMed PMID: 16306520
11. Raghu G, Anstrom KJ, King TE Jr, Lasky JA, Martinez FJ. Prednisone, azathioprine, and N-acetylcysteine for pulmonary fibrosis. N Engl J Med 2012;366(21):1968–77. PubMed PMID: 22607134
12. Martinez FJ, de Andrade JA, Anstrom KJ, King TE Jr, Raghu G. Randomized trial of acetylcysteine in idiopathic pulmonary fibrosis. N Engl J Med 2014;370(22):2093–101. PubMed PMID: 24836309
13. Oldham JM, Ma SF, Martinez FJ, Anstrom KJ, Raghu G, Schwartz DA, et al. TOLLIP, MUC5B, and the Response to N-Acetylcysteine among Individuals with Idiopathic Pulmonary Fibrosis. Am J Respir Crit Care Med 2015;192(12):1475–82. PubMed PMID: 26331942
14. Qi Q, Ailiyaer Y, Liu R, Zhang Y, Li C, Liu M, et al. Effect of N-acetylcysteine on exacerbations of bronchiectasis (BENE): a randomized controlled trial. Respir Res 2019;20(1):73. PubMed PMID: 30975143
15. De Flora S, Grassi C, Carati L. Attenuation of influenza-like symptomatology and improvement of cell-mediated immunity with long-term N-acetylcysteine treatment. Eur Respir J 1997;10(7):1535–41. PubMed PMID: 9230243
16. Geiler J, Michaelis M, Naczk P, Leutz A, Langer K, Doerr HW, et al. N-acetyl-L-cysteine (NAC) inhibits virus replication and expression of pro-inflammatory molecules in A549 cells infected with highly pathogenic H5N1 influenza A virus. Biochem Pharmacol 2010;79(3):413–20. PubMed PMID: 19732754
17. Cazzola M, Calzetta L, Page C, Jardim J, Chuchalin AG, Rogliani P, et al. Influence of N-acetylcysteine on chronic bronchitis or COPD exacerbations: a meta-analysis. Eur Respir Rev 2015;24(137):451–61. PubMed PMID: 26324807
18. Santus P, Corsico A, Solidoro P, Braido F, Di Marco F, Scichilone N. Oxidative stress and respiratory system: pharmacological and clinical reappraisal of N-acetylcysteine. COPD 2014;11(6):705–17. PubMed PMID: 24787454
19. Sadowska AM, Manuel-Y-Keenoy B, De Backer WA. Antioxidant and anti-inflammatory efficacy of NAC in the treatment of COPD: discordant in vitro and in vivo dose-effects: a review. Pulm Pharmacol Ther 2007;20(1):9–22. PubMed PMID: 16458553
20. Rushworth GF, Megson IL. Existing and potential therapeutic uses for N-acetylcysteine: the need for conversion to intracellular glutathione for antioxidant benefits. Pharmacol Ther 2014;141(2):150–9. PubMed PMID: 24080471
21. Dekhuijzen PN. Antioxidant properties of N-acetylcysteine: their relevance in relation to chronic obstructive pulmonary disease. Eur Respir J 2004;23(4):629–36. PubMed PMID: 15083766
22. Bridgeman MM, Marsden M, MacNee W, Flenley DC, Ryle AP. Cysteine and glutathione concentrations in plasma and bronchoalveolar lavage fluid after treatment with N-acetylcysteine. Thorax 1991;46(1):39–42. PubMed PMID: 1871695
23. Cantin AM, North SL, Hubbard RC, Crystal RG. Normal alveolar epithelial lining fluid contains high levels of glutathione. J Appl Physiol (1985) 1987;63(1):152–7. PubMed PMID: 3040659
24. Takeyama K, Dabbagh K, Jeong Shim J, Dao-Pick T, Ueki IF, Nadel JA. Oxidative stress causes mucin synthesis via transactivation of epidermal growth factor receptor: role of neutrophils. J Immunol 2000;164(3):1546–52. PubMed PMID: 10640773
25. Roum JH, Buhl R, McElvaney NG, Borok Z, Crystal RG. Systemic deficiency of glutathione in cystic fibrosis. J Appl Physiol (1985) 1993;75(6):2419–24. Search PubMed
26. Tam J, Nash EF, Ratjen F, Tullis E, Stephenson A. Nebulized and oral thiol derivatives for pulmonary disease in cystic fibrosis. Cochrane Database Syst Rev 2013;2013(7):CD007168. PubMed PMID: 23852992
27. Millman M, Millman FM, Goldstein IM, Mercandetti AJ. Use of acetylcysteine in bronchial asthma--another look. Ann Allergy 1985;54(4):294–6. PubMed PMID: 3985424
28. Aliyali M, Poorhasan Amiri A, Sharifpoor A, Zalli F. Effects of N-acetylcysteine on asthma exacerbation. Iran J Allergy Asthma Immunol 2010;9(2):103–9. PubMed PMID: 20683104
29. Ungheri D, Pisani C, Sanson G, Bertani A, Schioppacassi G, Delgado R, et al. Protective effect of n-acetylcysteine in a model of influenza infection in mice. Int J Immunopathol Pharmacol 2000;13(3):123–128. PubMed PMID: 12657201
30. Zhang Q, Ju Y, Ma Y, Wang T. N-acetylcysteine improves oxidative stress and inflammatory response in patients with community acquired pneumonia: A randomized controlled trial. Medicine (Baltimore) 2018;97(45):e13087. PubMed PMID: 30407312
31. Sharafkhah M, Abdolrazaghnejad A, Zarinfar N, Mohammadbeigi A, Massoudifar A, Abaszadeh S. Safety and efficacy of N-acetyl-cysteine for prophylaxis of ventilator-associated pneumonia: a randomized, double blind, placebo-controlled clinical trial. Med Gas Res 2018;8(1):19–23. PubMed PMID: 29770192
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33. Bernard GR, Wheeler AP, Arons MM, Morris PE, Paz HL, Russell JA, et al. A trial of antioxidants N-acetylcysteine and procysteine in ARDS. The Antioxidant in ARDS Study Group. Chest 1997;112(1):164–72. PubMed PMID: 9228372
34. Olsson B, Johansson M, Gabrielsson J, Bolme P. Pharmacokinetics and bioavailability of reduced and oxidized N-acetylcysteine. Eur J Clin Pharmacol 1988;34(1):77–82. PubMed PMID: 3360052
35. Horowitz JD, Henry CA, Syrjanen ML, Louis WJ, Fish RD, Smith TW, et al. Combined use of nitroglycerin and N-acetylcysteine in the management of unstable angina pectoris. Circulation 1988;77(4):787–94. PubMed PMID: 3127076

PubMed Topic Searches

Selected PubMed topic searches relevant to N-acetylcysteine in pulmonology, including COPD, pulmonary fibrosis, and cystic fibrosis.

1. PubMed: NAC in COPD exacerbations
2. PubMed: NAC in chronic bronchitis
3. PubMed: NAC in IPF (IFIGENIA/PANTHER)
4. PubMed: NAC in cystic fibrosis
5. PubMed: NAC and influenza/respiratory infection
6. PubMed: NAC and bronchiectasis
7. PubMed: NAC as a mucolytic
8. PubMed: NAC in asthma
9. PubMed: NAC in ARDS
10. PubMed: NAC, smoking, and lung oxidative stress
11. PubMed: Glutathione in airway epithelium
12. PubMed: Nebulized / inhaled NAC

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Connections

• Free Radicals & Your Antioxidant Network — interactive animation
• NAC Overview
• NAC & Glutathione
• COPD
• Asthma
• Cystic Fibrosis
• Influenza
• Pneumonia
• NAC & Mental Health
• Immune Boosting
• Cold & Flu Treatments
• Elderberry
• Oregano
• Eucalyptus
• Thyme
• Breathwork
• Oxidative Stress
• Cysteine

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