Acetyl Salicylic Acid: Uses, Properties, and Safety Precautions Explained

Few molecules in the pharmacopeia carry as much history, or as much unfinished science, as acetyl salicylic acid. First synthesized in a form suitable for medicine in the late nineteenth century, it has been in continuous clinical use for well over a century, and yet it keeps generating new research questions — about platelet biology, inflammation, and the boundary between benefit and bleeding risk. Almost every adult has taken it at some point. Very few have been asked to think about it as what it fundamentally is: a small, structurally elegant ester whose chemistry explains nearly everything about how it works, how it fails, and why it needs careful handling.

This guide examines acetyl salicylic acid the way a pharmaceutical scientist would: starting from its chemical structure and structural formula, moving through its physical and chemical properties, its mechanism of action and clinical uses, the impurity and stability behavior that quality control laboratories must manage, and the safety precautions that apply both to patients and to anyone handling the material at scale.

What Is Acetyl Salicylic Acid?

Acetyl salicylic acid (ASA), widely known as aspirin (originally a Bayer trade name, and still a registered trademark in some countries), is the acetyl ester of salicylic acid, formally named 2-acetoxybenzoic acid under IUPAC nomenclature.

It answers one specific question: What is this molecule, structurally and functionally?

ASA is a non-steroidal anti-inflammatory drug (NSAID) with a combination of pharmacological activities that few other agents share: analgesic, antipyretic, anti-inflammatory, and — uniquely among common NSAIDs at low dose — durable antiplatelet activity. That last property is a direct consequence of a specific chemical feature, the reactive acetyl group, discussed in detail below.

Quick identification reference:

Property	Value
IUPAC name	2-Acetoxybenzoic acid (2-acetyloxybenzoic acid)
Common names	Acetylsalicylic acid, ASA, aspirin
CAS number	50-78-2
Molecular formula	C₉H₈O₄
Molar mass	180.16 g/mol
SMILES	CC(=O)Oc1ccccc1C(=O)O
Functional groups	Carboxylic acid, aryl ester (acetate), benzene ring
Drug class	Non-steroidal anti-inflammatory drug (NSAID); antiplatelet agent

Acetyl Salicylic Acid Structure: The Chemical Structure and Structural Formula Explained

Understanding the acetyl salicylic acid chemical structure is not an academic exercise. Every property that matters in practice — acidity, solubility, stability, mechanism of action, and the impurity profile that quality laboratories monitor — traces directly back to how a handful of atoms are arranged on a benzene ring.

The structural formula for acetyl salicylic acid

The structural formula can be written in condensed form as:

CH₃–CO–O–C₆H₄–COOH (with the two substituents in the ortho, or 1,2, relationship on the benzene ring)

Equivalently, it can be written as C₆H₄(OCOCH₃)(COOH), and the molecular formula is C₉H₈O₄. In words, the molecule consists of a benzene ring carrying two adjacent substituents: a carboxylic acid group (–COOH) at one position, and an acetoxy group (–OCOCH₃, an acetate ester linked through oxygen to the ring) at the neighboring position.

This is why ASA is described as "the acetate ester of salicylic acid." Salicylic acid is 2-hydroxybenzoic acid, carrying a free phenolic –OH group ortho to the carboxylic acid. Acetylation of that phenolic hydroxyl converts it to the acetate ester, giving acetyl salicylic acid.

Key structural features:

• Aromatic benzene core — a planar, delocalized ring system that provides a rigid scaffold and is largely responsible for the molecule's UV absorbance and its moderate lipophilicity
• Carboxylic acid group — the ionizable function, with a pKa of approximately 3.5, meaning ASA is a considerably stronger acid than acetic acid and exists predominantly as the anionic carboxylate at physiological pH
• Aryl acetate ester — the group responsible both for ASA's pharmacological distinctiveness (it can transfer its acetyl group to nucleophilic residues in proteins) and for its principal chemical weakness (it is susceptible to hydrolysis)
• Ortho relationship of the two substituents — the proximity of the carboxylic acid and the ester is not incidental; it allows intramolecular participation of the neighboring carboxylate in ester hydrolysis, which helps explain why ASA is more moisture-sensitive than a simple aryl acetate
• No phenolic –OH — in contrast to salicylic acid, the phenol is masked as an ester, which changes the molecule's hydrogen-bonding behavior, its irritancy profile, and its pharmacology

Solid-state structure

In the crystalline state, ASA molecules typically associate through hydrogen-bonded carboxylic acid dimers, a common motif for carboxylic acids. ASA is also known to exhibit polymorphism, with a well-characterized stable form (Form I) and a second form (Form II) described in the crystallographic literature. For pharmaceutical purposes, the practical relevance is that solid-state form can influence dissolution and compaction behavior, which is why solid-state characterization (XRPD, DSC) is part of thorough drug substance characterization.

Why the structural distinction matters?

The structure explains four behaviors that dominate everything else in this article. The ester explains reactivity: it hydrolyzes in the presence of moisture to give salicylic acid and acetic acid, the origin of the vinegar odor in aged aspirin. The same ester explains pharmacology: it acetylates a serine residue at the active site of cyclooxygenase. The carboxylic acid explains acidity, ionization, and gastric behavior. And the aromatic ring explains the analytical handle, since ASA and its aromatic impurities absorb UV light and are readily detected by HPLC-UV.

The structure is not decoration. It is the reason ASA works, the reason it degrades, and the reason it demands the quality controls it receives.

Physical and Chemical Properties of Acetyl Salicylic Acid

Physical properties

Property	Value
Appearance	White, crystalline powder or colorless crystals
Odor	Odorless when pure; vinegar-like odor on degradation (acetic acid)
Melting point	Approximately 135–136°C (about 143°C by the instantaneous method; decomposition occurs near and above the melting range)
Density	~1.40 g/cm⊃3;
Water solubility	~3 g/L at 20°C (sparingly soluble; increases with temperature)
Solubility in organic solvents	Soluble in ethanol; soluble in chloroform and diethyl ether to varying degrees
pKa	~3.5 (carboxylic acid)
Log P (octanol/water)	~1.2 (moderate lipophilicity)
UV absorbance	Characteristic absorbance in the UV region, supporting HPLC-UV detection

Note that the melting point of ASA is reported with some variability in the literature, because the compound begins to decompose as it melts. For this reason, melting point alone is a weak identity test for ASA, and compendial methods rely on spectroscopic and chromatographic confirmation.

Chemical properties and reactivity

Property/Behavior	Description
Hydrolytic instability	The aryl ester hydrolyzes to salicylic acid and acetic acid; rate increases with moisture, temperature, and alkaline pH
Acid–base behavior	Moderately strong organic acid; forms water-soluble salts (e.g., sodium, calcium, lysine) with bases
Acetylating ability	Can transfer its acetyl group to nucleophiles such as serine hydroxyl groups in proteins
Thermal behavior	Decomposes near its melting point; sensitive to prolonged heat exposure
Incompatibilities	Alkaline excipients (e.g., magnesium oxide, some carbonates), moisture-rich excipients, and certain amine-containing drugs can accelerate degradation or react directly
Light sensitivity	Relatively stable to light compared with its moisture sensitivity; protection from humidity is the primary storage concern

Mechanism of Action: Why the Acetyl Group Matters

ASA's pharmacology is a direct consequence of its structure, and understanding it clarifies both its clinical uses and its safety profile.

Cyclooxygenase (COX) enzymes convert arachidonic acid to prostaglandin H₂, the precursor of prostaglandins and thromboxane A₂. Most NSAIDs inhibit COX reversibly by occupying the active-site channel. ASA is different: it acts as an acetylating agent, transferring its acetyl group to a specific serine residue within the COX active-site channel (Ser529 in human COX-1, often cited as Ser530 using the ovine numbering, and Ser516 in human COX-2). This covalent modification blocks access of arachidonic acid to the catalytic site and is effectively irreversible for the lifetime of that enzyme molecule. ASA is considerably more potent against COX-1 than COX-2, and acetylated COX-2 is not completely inactivated: it switches to producing 15(R)-HETE, the precursor of the so-called aspirin-triggered lipoxins.

This irreversible mechanism has a consequential implication for platelets. Mature platelets lack a nucleus and therefore cannot synthesize new COX-1 protein. Once a platelet's COX-1 has been acetylated, that platelet cannot produce thromboxane A₂ for the remainder of its lifespan, which is on the order of 7 to 10 days. The antiplatelet effect of even a low dose of ASA therefore outlasts the drug's own short plasma half-life, and recovery of platelet function depends on the production of new platelets. Nucleated cells in the vascular wall, by contrast, can resynthesize COX, which is part of why low-dose regimens can preferentially affect platelet thromboxane production. In addition, an oral low dose acetylates platelet COX-1 in the portal circulation before ASA is hydrolyzed to salicylic acid during first-pass metabolism, which further favors the effect on platelets.

Dose–response relationship at a glance

Dose Range (typical adult)	Dominant Pharmacological Effect	Common Clinical Context
Low dose (~75–100 mg/day)	Antiplatelet (COX-1 inhibition in platelets, reduced thromboxane A₂)	Secondary prevention of cardiovascular events
Moderate dose (~325–1000 mg per dose)	Analgesic and antipyretic	Mild-to-moderate pain, fever
High dose (multi-gram daily, under medical supervision)	Anti-inflammatory	Historically used in inflammatory arthritis; largely replaced by newer agents

Uses of Acetyl Salicylic Acid

Clinical and therapeutic uses

• Secondary prevention of atherothrombotic events — low-dose ASA is well established for patients with prior myocardial infarction, ischemic stroke, or established cardiovascular disease, where the antiplatelet benefit generally outweighs bleeding risk
• Acute coronary syndromes — ASA is a standard early component of treatment for suspected acute myocardial infarction
• Analgesia and antipyresis — for mild-to-moderate pain (headache, musculoskeletal pain, dental pain) and fever in adults
• Anti-inflammatory therapy — historically important in rheumatic conditions, though now less commonly the first choice because of tolerability considerations
• Primary prevention — the role of ASA for primary prevention of cardiovascular disease in people without established disease has been substantially re-evaluated, and current guidance in many jurisdictions is considerably more restrictive than in the past because bleeding risk offsets modest benefit in many populations; this is a decision for clinicians, not for self-treatment

Pharmaceutical and industrial uses

• Drug substance for finished dosage forms — immediate-release and enteric-coated tablets, effervescent and chewable formulations, and fixed-dose combinations
• Reference and working standard material — in analytical laboratories, ASA is used as a reference material in assay and related-substances methods, and its principal degradation products serve as impurity reference standards
• Synthetic precursor and model compound — ASA synthesis from salicylic acid and acetic anhydride is a staple of teaching laboratories because it cleanly demonstrates esterification, recrystallization, and purity assessment by melting point and spectroscopy

Synthesis and degradation at a glance

The same chemistry that makes ASA is the chemistry that unmakes it. The diagram below shows the forward synthesis and the reverse hydrolytic degradation pathway.

The loop in this diagram carries a quality implication: free salicylic acid appears in ASA drug substance both as a process-related impurity (unreacted starting material) and as a degradation impurity (formed on storage), which makes it the single most important related substance to control.

Impurities and Stability: What Quality Laboratories Monitor

Because ASA hydrolyzes readily, impurity and stability control is central to its quality profile.

Impurity / Degradant	Origin	Why It Matters
Salicylic acid	Unreacted starting material; hydrolytic degradation product (Ph. Eur. Impurity C)	Primary controlled impurity; tightly limited in pharmacopeial specifications; irritant and associated with discoloration
Acetic acid	Hydrolytic degradation product	Source of vinegar odor; indicator of moisture-driven degradation
Acetylsalicylsalicylic acid (Impurity D) and salicylsalicylic acid / salsalate (Impurity E)	Self-esterification side reactions during synthesis	Process-related impurities requiring chromatographic resolution and control
Acetylsalicylic anhydride (Impurity F)	By-product of acetylation with acetic anhydride	Process-related; controlled at low levels because anhydride-type impurities have been linked to hypersensitivity reactions
4-Hydroxybenzoic acid (Impurity A) and 4-hydroxyisophthalic acid (Impurity B)	Carried over from the salicylic acid starting material (Kolbe–Schmitt carboxylation by-products)	Starting-material quality markers
Residual solvents	Crystallization and purification steps	Controlled under ICH Q3C
Elemental impurities	Catalysts, equipment	Assessed under ICH Q3D risk-based approach

Pharmacopeial monographs set tight limits for free salicylic acid in the drug substance (in the range of about 0.1–0.15%, depending on the pharmacopoeia; consult the current USP/EP text for the exact specification) and separate, typically higher, limits for finished tablets, reflecting the fact that some hydrolysis during manufacturing and shelf life is unavoidable.

Analytical approach in brief

HPLC with UV detection is the standard approach for assay and related substances. Method development has to address a practical difficulty: ASA can hydrolyze during sample preparation, so diluent choice, solution stability, and analysis timing must be controlled to avoid artificially inflating the measured salicylic acid level. Forced degradation studies (acid, base, oxidative, thermal, humidity) confirm that the method is stability-indicating. Chemicea Pharmaceuticals supports this work with characterized reference standards for ASA-related impurities, enabling accurate identification and quantification rather than reliance on area-percent estimates alone.

Regulatory Framework — What Specifically Applies

Regulatory Document	Governs	Relevance to ASA
USP / EP / BP / JP monographs	Identity, assay, impurity limits, tests for drug substance and dosage forms	Define compendial specifications for ASA and its tablets
ICH Q3A / Q3B	Impurities in new drug substances and products	Framework for reporting, identification and qualification; formally written for new drug substances and applied by analogy to established APIs such as ASA, together with the pharmacopoeial monographs
ICH Q3C	Residual solvents	Crystallization/purification solvent limits
ICH Q3D	Elemental impurities	Risk assessment of catalyst/equipment-derived metals
ICH Q1A(R2)	Stability testing	Long-term and accelerated studies, critical given hydrolytic sensitivity
ICH Q2(R2)	Analytical procedure validation	Validation of assay and related-substances methods
ICH Q7	GMP for APIs	Manufacturing controls for ASA drug substance
FDA OTC monograph (now final administrative orders under the 2020 OTC Monograph Reform) and national labeling requirements	Labeling, warnings, permitted indications	Includes warnings related to Reye's syndrome and bleeding

One practical point: because ASA is widely sold over the counter, labeling and warning requirements are as heavily regulated as manufacturing quality, and product labels must carry specific warnings that reflect the safety profile discussed in the next section.

Safety Precautions for Acetyl Salicylic Acid

Safety considerations for ASA fall into two distinct groups: clinical (patient) safety and occupational (handling) safety. Both matter for a complete picture.

Clinical safety considerations

Risk	Description	Key Precaution
Gastrointestinal irritation and bleeding	ASA inhibits protective gastric prostaglandins and impairs platelet function, increasing risk of ulceration and bleeding	Use the lowest effective dose; caution in those with ulcer history, anticoagulant use, heavy alcohol use, or advanced age
Bleeding risk	Irreversible platelet inhibition prolongs bleeding time for days	Disclose use before surgery or dental procedures; avoid unsupervised combination with anticoagulants or other NSAIDs
Reye's syndrome	A rare but serious condition (acute encephalopathy with liver involvement) associated with ASA use during viral illness in children and adolescents	Generally avoid ASA in children and teenagers with viral infections such as influenza or chickenpox, unless specifically directed by a physician; in the UK, ASA is not recommended for anyone under 16 unless prescribed
Hypersensitivity and asthma	Some individuals, particularly those with asthma, nasal polyps, or chronic rhinosinusitis, experience bronchospasm or other reactions, a condition known as aspirin-exacerbated respiratory disease (AERD)	Avoid in individuals with known ASA or NSAID hypersensitivity
Salicylate toxicity (salicylism)	Overdose causes tinnitus, nausea, hyperventilation, and metabolic disturbance, and can be life-threatening	Observe dose limits; seek emergency care for suspected overdose
Pregnancy	Analgesic and anti-inflammatory doses, like other NSAIDs, should be avoided from about 20 weeks of gestation and are contraindicated in the third trimester (effects on the fetal ductus arteriosus and kidneys, bleeding at delivery). Low-dose ASA is, however, recommended under medical supervision for pregnant women at high risk of pre-eclampsia	Use in pregnancy only as directed by a clinician
Drug interactions	Interactions with anticoagulants, other NSAIDs, SSRIs, methotrexate, certain antihypertensives, and others; ibuprofen taken shortly before low-dose ASA can block its antiplatelet effect	Review the full medication list with a pharmacist or physician

These points are general educational information and not individual medical advice. Anyone with a medical condition, anyone taking other medications, and any parent considering ASA for a child should consult a qualified healthcare professional.

Occupational and laboratory handling safety

For laboratories and manufacturing sites handling ASA as a bulk powder, the principal hazards are modest compared with highly reactive solvents, but they are real:

• Dust exposure — fine ASA dust can irritate the eyes, nose, and respiratory tract, and can provoke reactions in sensitized individuals; handle with local exhaust ventilation or in a ventilated enclosure, and use appropriate respiratory protection when dust generation is unavoidable
• Skin and eye contact — wear gloves and eye protection; rinse promptly on contact
• Combustible dust — like many fine organic powders, ASA dust dispersed in air can present a dust-explosion hazard under the right conditions; minimize dust accumulation and control ignition sources
• Ingestion — classified under GHS as Acute Toxicity Category 4 (H302, harmful if swallowed); prohibit eating and drinking in handling areas
• Sensitization — individuals with known salicylate hypersensitivity should avoid occupational exposure

Storage and stability precautions

Storage Consideration	Recommended Practice
Moisture	Store in tightly closed containers in a dry environment; humidity is the principal driver of degradation
Temperature	Cool, controlled room temperature; avoid prolonged heat exposure
Packaging	Use moisture-protective primary packaging (e.g., low-permeability containers, desiccant where justified)
Excipient compatibility	Avoid strongly alkaline or hygroscopic excipients in formulations; verify compatibility early in development
Inspection	Treat a strong vinegar odor as a sign of degradation; investigate and test before use
Labeling and dating	Record date received and opened; apply first-expired, first-out inventory control

A Worked Example: Tracing a Rising Salicylic Acid Level

Consider a quality control laboratory running routine stability testing on enteric-coated ASA tablets. At the 6-month accelerated timepoint, free salicylic acid has risen well above its release value, and the sample bottles have a faint vinegar odor.

A disciplined investigation separates the possible causes. First, is the salicylic acid increase real, or an analytical artifact? Because ASA can hydrolyze in solution, the team re-prepares samples with a fresh, appropriately acidified or non-aqueous diluent, injects promptly, and checks solution stability, confirming whether the measured increase reflects true degradation in the tablet or hydrolysis occurring after sample preparation.

Having confirmed the increase is real, the team turns to root cause. The vinegar odor — acetic acid — points toward hydrolytic degradation rather than a synthetic carryover, since unreacted salicylic acid would not generate acetic acid on storage. The team then examines moisture exposure: packaging water-vapor transmission, desiccant performance, and the moisture content of excipients at the time of manufacture. Finally, compatibility is reviewed, since an alkaline lubricant or filler can locally accelerate ester hydrolysis in the tablet microenvironment.

The resolution might be a packaging change, a tighter excipient moisture specification, or a formulation adjustment. Notice that identifying the right reference standards — salicylic acid for quantification and, where needed, related dimeric impurities — is what allows the team to attribute the peak correctly rather than guess. This is exactly the kind of work where well-characterized reference materials from a supplier such as Chemicea Pharmaceuticals shorten the investigation.

Comparison: Acetyl Salicylic Acid vs. Related Analgesics

Property	Acetyl Salicylic Acid	Salicylic Acid	Paracetamol (Acetaminophen)	Ibuprofen
Structure type	Aryl acetate ester of salicylic acid	Phenolic acid	p-Aminophenol derivative (N-acetyl-p-aminophenol)	Arylpropionic acid
COX inhibition	Irreversible (acetylation)	Weak/indirect	Weak peripheral; central mechanisms	Reversible
Antiplatelet effect	Durable (platelet lifetime)	Minimal	Negligible	Reversible, short-lived
Anti-inflammatory activity	Yes	Yes when given systemically as salicylate (weak COX inhibitor); used topically as a keratolytic	Minimal	Yes
Main safety concerns	GI bleeding, bleeding risk, Reye's syndrome, hypersensitivity	Local irritation; toxic if ingested in quantity	Hepatotoxicity in overdose	GI and cardiovascular risk
Hydrolytic stability	Poor (ester)	Stable	Good (amide); 4-aminophenol is the key degradant	Stable

This comparison highlights why ASA is unique among common analgesics: it is the only one in the group that irreversibly modifies its target enzyme, and the only one whose principal quality challenge is hydrolysis of an ester linkage.

Common Pitfalls in Handling and Quality Control of Acetyl Salicylic Acid

Treating melting point as a sufficient identity or purity test. Because ASA decomposes near its melting range, melting point is a weak discriminator; compendial identity relies on IR and chromatographic confirmation.

Ignoring solution stability during analysis. Preparing standards and samples in unsuitable diluents or allowing solutions to stand can generate salicylic acid in the vial, producing false impurity results and unnecessary out-of-specification investigations.

Underestimating excipient interactions. Alkaline or moisture-rich excipients can accelerate hydrolysis, and compatibility studies performed late in development often find problems that early screening would have caught.

Assuming over-the-counter status means low risk. ASA's availability without prescription does not remove its bleeding, hypersensitivity, and Reye's syndrome considerations, nor does it reduce the need for rigorous manufacturing and labeling controls.

Neglecting dust control in bulk handling. Fine ASA powder is both an irritant and, under the right conditions, a combustible dust, and housekeeping failures in powder-handling areas are a recurring cause of avoidable incidents.

Failing to distinguish process-related from degradation-related salicylic acid. The same impurity can arise from two different causes, and the corrective action differs: synthetic route and purification improvements for the former, packaging and formulation changes for the latter.

Conclusion

Acetyl salicylic acid is a case study in how a molecule's structure determines its fate. A benzene ring, a carboxylic acid, and an adjacent acetate ester — a structural formula that fits on a single line — account for its irreversible inhibition of cyclooxygenase, its distinctive antiplatelet profile, its moderate acidity, its sensitivity to moisture, and the impurity profile that quality laboratories track so carefully. The same acetyl group that gives ASA its pharmacological uniqueness is the group that hydrolyzes on the shelf, which is why storage, packaging, and analytical method design are core elements of its quality strategy rather than afterthoughts.

Respecting ASA means holding two ideas at once: it is a remarkably effective and well-studied therapeutic agent, and it is a molecule with real, structure-driven risks, both for patients and for the people who manufacture and test it. Laboratories and manufacturers that understand the underlying chemistry, rather than only following a checklist, are better positioned to prevent degradation, resolve out-of-specification results quickly, and produce material that meets its specification throughout its shelf life.

Frequently Asked Questions

Q1: What is the chemical structure of acetyl salicylic acid?

Acetyl salicylic acid consists of a benzene ring carrying a carboxylic acid group (–COOH) and an acetoxy group (–OCOCH₃) on adjacent (ortho) carbons. Its condensed structural formula is CH₃–CO–O–C₆H₄–COOH, its molecular formula is C₉H₈O₄, and its molar mass is approximately 180.16 g/mol.

Q2: What is the structural formula for acetyl salicylic acid, and how does it differ from salicylic acid?

The structural formula is CH₃COO–C₆H₄–COOH. Salicylic acid (2-hydroxybenzoic acid) has a free phenolic –OH group ortho to the carboxylic acid; acetylation of that –OH produces the acetate ester, which is acetyl salicylic acid. This small change alters the molecule's pharmacology, irritancy, and stability.

Q3: Why does aspirin smell like vinegar when it ages?

Acetyl salicylic acid hydrolyzes in the presence of moisture to yield salicylic acid and acetic acid. Acetic acid is the main component of vinegar, so a vinegar-like odor indicates that degradation has occurred and the material should be tested before use.

Q4: How does acetyl salicylic acid work as an antiplatelet agent?

It irreversibly acetylates a serine residue in the active site of cyclooxygenase-1 in platelets, blocking production of thromboxane A₂. Because platelets cannot synthesize new enzyme, the effect lasts for the platelet's lifespan of roughly 7 to 10 days, which is why even low daily doses produce a sustained antiplatelet effect.

Q5: Why is salicylic acid the most important impurity in acetyl salicylic acid?

Free salicylic acid arises both as unreacted starting material from synthesis and as the primary hydrolytic degradation product on storage. It is therefore tightly controlled in pharmacopeial specifications and is the key marker of both process quality and stability.

Q6: Why is aspirin generally avoided in children and teenagers with viral illnesses?

Its use during viral infections such as influenza or chickenpox has been associated with Reye's syndrome, a rare but serious condition affecting the brain and liver. Parents and caregivers should consult a physician or pharmacist before giving aspirin or any salicylate-containing product to a child or adolescent.

Q7: What are the main laboratory handling precautions for bulk acetyl salicylic acid?

Control dust with local exhaust ventilation or a ventilated enclosure, wear gloves and eye protection, avoid ingestion and inhalation, minimize dust accumulation because fine organic powders can be combustible, and store the material in tightly closed containers in a dry environment to prevent hydrolysis. Always consult the current Safety Data Sheet and the site's chemical hygiene plan.